J Asthma. Allen S, Britton JR, Leonardi-Bee JA. Association between antioxidant vitamins and asthma outcome measures: systematic review and meta-analysis.

Cui W, Zhang P, Gu J, Tian Y, Gao X, Liu Y, et al. Vitamin A deficiency promotes inflammation by induction of type 2 cytokines in experimental ovalbumin-induced asthma murine model.

Hall JA, Grainger JR, Spencer SP, Belkaid Y. The role of retinoic acid in tolerance and immunity. Kheirouri S, Alizadeh M. Decreased serum and mucosa immunoglobulin a levels in vitamin a- and zinc-deficient mice.

Cent Eur J Immunol. Penkert RR, Smith AP, Hrincius ER, McCullers JA, Vogel P, Smith AM, et al. Effect of vitamin A deficiency in dysregulating immune responses to influenza virus and increasing mortality rates after bacterial coinfections. J Infect Dis.

Hemilä H, Louhiala P. Vitamin C for preventing and treating pneumonia. Cochrane Database Syst Rev. Dogan P, Ozkan H, Koksal N, Bagci O, Varal IG. Vitamin d deficiency and its effect on respiratory distress syndrome in premature infants: results from a prospective study in a tertiary care centre.

Afr Health Sci. Greiller CL, Martineau AR. Modulation of the immune response to respiratory viruses by vitamin D. Yim S, Dhawan P, Ragunath C, Christakos S, Diamond G.

Induction of cathelicidin in normal and CF bronchial epithelial cells by 1,dihydroxyvitamin D3. J Cyst Fibros.

Wang T-T, Nestel FP, Bourdeau V, Nagai Y, Wang Q, Liao J, et al. Cutting edge: 1,Dihydroxyvitamin D 3 is a direct inducer of antimicrobial peptide gene expression.

Currie SM, Findlay EG, McHugh BJ, Mackellar A, Man T, Macmillan D, et al. The human cathelicidin LL has antiviral activity against respiratory syncytial virus. Belderbos ME, Houben ML, Wilbrink B, Lentjes E, Bloemen EM, Kimpen JLL, et al. Cord blood vitamin D deficiency is associated with respiratory syncytial virus bronchiolitis.

Khare D, Godbole NM, Pawar SD, Mohan V, Pandey G, Gupta S, et al. Calcitriol [1, 25[OH]2 D3] pre- and post-treatment suppresses inflammatory response to influenza A H1N1 infection in human lung A epithelial cells. Eur J Nutr. Shimosawa T, Takano K, Ando K, Fujita T.

Magnesium inhibits norepinephrine release by blocking N-type calcium channels at peripheral sympathetic nerve endings. Baker JC, Tunnicliffe WS, Duncanson RC, Ayres JG. Dietary antioxidants and magnesium in type 1 brittle asthma: a case control study.

Fogarty A, Lewis SA, Scrivener SL, Antoniak M, Pacey S, Pringle M, et al. Oral magnesium and vitamin C supplements in asthma: a parallel group randomized placebo-controlled trial. Misso NLA, Peroni DJ, Neil Watkins D, Stewart GA, Thompson PJ. Glutathione peroxidase activity and mRNA expression in eosinophils and neutrophils of asthmatic and non-asthmatic subjects.

J Leukoc Biol. Kadrabová J, Mad'arič A, Kovačiková Z, Podivínsky F, Ginter E, Gazdík F. Selenium status is decreased in patients with intrinsic asthma. Biol Trace Elem Res. Shaheen SO, Newson RB, Rayman MP, Wong APL, Tumilty MK, Phillips JM, et al. Randomised, double blind, placebo-controlled trial of selenium supplementation in adult asthma.

Hijazi N, Abalkhail B, Seaton A. Diet and childhood asthma in a society in transition: a study in urban and rural Saudi Arabia. Burney P, Potts J, Makowska J, Kowalski M, Phillips J, Gnatiuc L, et al.

A case-control study of the relation between plasma selenium and asthma in European populations: a GA2LEN project. Kirkil G, Hamdi Muz M, Seçkin D, Sahin K, Küçük Ö. Antioxidant effect of zinc picolinate in patients with chronic obstructive pulmonary disease.

Respir Med. Bhandari N, Bahl R, Taneja S, Strand T, Mølbak K, Ulvik RJ, et al. Effect of routine zinc supplementation on pneumonia in children aged 6 months to 3 years: randomised controlled trial in an urban slum.

Br Med J. Sazawal S, Jalla S, Mazumder S, Sinha A, Black RE, Bhan MK. Effect of zinc supplementation on cell-mediated immunity and lymphocyte subsets in preschool children. Indian Pediatr. Shankar AH, Prasad AS.

Zinc and immune function: the biological basis of altered resistance to infection. Am J Clin Nutr. Shi L, Zhang L, Li C, Hu X, Wang X, Huang Q, et al. te Velthuis AJW, van den Worml SHE, Sims AC, Baric RS, Snijder EJ, van Hemert MJ.

Muckenthaler MU, Rivella S, Hentze MW, Galy B. A red carpet for iron metabolism. Papanikolaou G, Pantopoulos K.

Iron metabolism and toxicity. Toxicol Appl Pharmacol. Neves J, Haider T, Gassmann M, Muckenthaler MU. Iron homeostasis in the lungs—a balance between health and disease.

Gupta SC, Tyagi AK, Deshmukh-Taskar P, Hinojosa M, Prasad S, Aggarwal BB. Downregulation of tumor necrosis factor and other proinflammatory biomarkers by polyphenols.

Arch Biochem Biophys. Singh B, Kumar A, Malik AK. Flavonoids biosynthesis in plants and its further analysis by capillary electrophoresis. Wang TY, Li Q, Bi KS. Bioactive flavonoids in medicinal plants: structure, activity and biological fate.

Asian J Pharm Sci. Manach C, Scalbert A, Morand C, Rémésy C, Jiménez L. Polyphenols: food sources and bioavailability. Thilakarathna SH, Vasantha Rupasinghe HP. Flavonoid bioavailability and attempts for bioavailability enhancement.

Lolli G, Cozza G, Mazzorana M, Tibaldi E, Cesaro L, Donella-Deana A, et al. Inhibition of protein kinase CK2 by flavonoids and tyrphostins. A structural insight.

Chen L, Teng H, Jia Z, Battino M, Miron A, Yu Z, et al. Intracellular signaling pathways of inflammation modulated by dietary flavonoids: the most recent evidence. Crit Rev Food Sci Nutr. Maleki SJ, Crespo JF, Cabanillas B.

Anti-inflammatory effects of flavonoids. Food Chem. Pinho-Ribeiro FA, Zarpelon AC, Mizokami SS, Borghi SM, Bordignon J, Silva RL, et al.

The citrus flavonone naringenin reduces lipopolysaccharide-induced inflammatory pain and leukocyte recruitment by inhibiting NF-κB activation. J Nutr Biochem. Peng HL, Huang WC, Cheng SC, Liou CJ.

Int Immunopharmacol. Manchope MF, Calixto-Campos C, Coelho-Silva L, Zarpelon AC, Pinho-Ribeiro FA, Georgetti SR, et al. Naringenin inhibits superoxide anion-induced inflammatory pain: role of oxidative stress, cytokines, Nrf-2 and the no-cGMP-PKG-KATP channel signaling pathway.

Hu QH, Zhang X, Pan Y, Li YC, Kong LD. Allopurinol, quercetin and rutin ameliorate renal NLRP3 inflammasome activation and lipid accumulation in fructose-fed rats.

Biochem Pharmacol. Yi YS. Regulatory roles of flavonoids on inflammasome activation during inflammatory responses. Mol Nutr Food Res.

Comalada M, Ballester I, Bailón E, Sierra S, Xaus J, Gálvez J, et al. Inhibition of pro-inflammatory markers in primary bone marrow-derived mouse macrophages by naturally occurring flavonoids: analysis of the structure-activity relationship.

Matsuda H, Nakamura S, Yoshikawa M. Degranulation inhibitors from medicinal plants in antigen-stimulated rat basophilic leukemia RBL-2H3 cells.

Chem Pharm Bull. Somerville VS, Braakhuis AJ, Hopkins WG. Effect of flavonoids on upper respiratory tract infections and immune function: a systematic review and meta-analysis.

Adv Nutr. Dhingra D, Michael M, Rajput H, Patil RT. Dietary fibre in foods: a review. J Food Sci Technol. Hanson C, Lyden E, Rennard S, Mannino DM, Rutten EPA, Hopkins R, et al. The relationship between dietary fiber intake and lung function in the national health and nutrition examination surveys.

Ann Am Thorac Soc. Young RP, Hopkins RJ, Marsland B. The gut-liver-lung axis: modulation of the innate immune response and its possible role in chronic obstructive pulmonary disease. Huffnagle GB. Increase in dietary fiber dampens allergic responses in the lung. European Food Safety Authority.

Scientific opinion on dietary reference values for carbohydrates and dietary fibre. EFSA J. Pal J, Shukla BN, Maurya AK, Verma HO.

A review on role of fish in human nutrition with special emphasis to essential fatty acid. Int J Fish Acquat Stud. Balić A, Vlašić D, ŽuŽul K, Marinović B, Mokos ZB. Omega-3 versus omega-6 polyunsaturated fatty acids in the prevention and treatment of inflammatory skin diseases.

Int J Mol Sci. Wendell SG, Baffi C, Holguin F. Fatty acids, inflammation, and asthma. Horrobin DF. Low prevalences of coronary heart disease CHD , psoriasis, asthma and rheumatoid arthritis in eskimos: are they caused by high dietary intake of eicosapentaenoic acid EPA , a genetic variation of essential fatty acid EFA metabolism or a combination of.

Med Hypotheses. Hinojosa CA, Gonzalez-Juarbe N, Rahman MM, Fernandes G, Orihuela CJ, Restrepo MI. Omega-3 fatty acids in contrast to omega-6 protect against pneumococcal pneumonia. Microb Pathog. Anand S, Mande SS. Diet, microbiota and gut-lung connection. Front Microbiol. Marsland BJ, Trompette A, Gollwitzer ES.

The gut-lung axis in respiratory disease. Belkaid Y, Hand TW. Role of the microbiota in immunity and inflammation. Brownawell AM, Caers W, Gibson GR, Kendall CWC, Lewis KD, Ringel Y, et al.

Prebiotics and the health benefits of fiber: current regulatory status, future research, and goals. Fragkou PC, Karaviti D, Zemlin M, Skevaki C.

Impact of early life nutrition on children's immune system and noncommunicable diseases through its effects on the bacterial microbiome, virome and mycobiome. Savage DC. Microbial ecology of the gastrointestinal tract.

Annu Rev Microbiol. Sender R, Fuchs S, Milo R. Revised estimates for the number of human and bacteria cells in the body. PLoS Biol. Bingula R, Filaire M, Radosevic-Robin N, Bey M, Berthon JY, Bernalier-Donadille A, et al.

Desired turbulence? Gut-Lung axis, immunity, and lung cancer. J Oncol. Souza DG, Vieira AT, Soares AC, Pinho V, Nicoli JR, Vieira LQ, et al. The essential role of the intestinal microbiota in facilitating acute inflammatory responses.

Maslowski KM, Vieira AT, Ng A, Kranich J, Sierro F, Di Yu, et al. Regulation of inflammatory responses by gut microbiota and chemoattractant receptor GPR de Souza Vieira R, Castoldi A, Basso PJ, Hiyane MI, Saraiva Câmara NO, Almeida RR.

Butyrate attenuates lung inflammation by negatively modulating Th9 cells. Theiler A, Bärnthaler T, Platzer W, Richtig G, Peinhaupt M, Rittchen S, et al.

Butyrate ameliorates allergic airway inflammation by limiting eosinophil trafficking and survival. Ruane D, Chorny A, Lee H, Faith J, Pandey G, Shan M, et al. Microbiota regulate the ability of lung dendritic cells to induce IgA class-switch recombination and generate protective gastrointestinal immune responses.

J Exp Med. Albenberg LG, Wu GD. Diet and the intestinal microbiome: associations, functions, and implications for health and disease. Walker AW, Ince J, Duncan SH, Webster LM, Holtrop G, Ze X, et al. Dominant and diet-responsive groups of bacteria within the human colonic microbiota. ISME J. Timmerman HM, Rutten NBMM, Boekhorst J, Saulnier DM, Kortman GAM, Contractor N, et al.

Intestinal colonisation patterns in breastfed and formula-fed infants during the first 12 weeks of life reveal sequential microbiota signatures. Alberca RW, Oliveira L de M, Branco ACCC, Pereira NZ, Sato MN.

Obesity as a risk factor for COVID an overview. Gensollen T, Iyer SS, Kasper DL, Blumberg RS. How colonization by microbiota in early life shapes the immune system.

Ekmekciu I, von Klitzing E, Fiebiger U, Escher U, Neumann C, Bacher P, et al. Immune responses to broad-spectrum antibiotic treatment and fecal microbiota transplantation in mice. Negi S, Pahari S, Bashir H, Agrewala JN.

Gut microbiota regulates mincle mediated activation of lung dendritic cells to protect against mycobacterium tuberculosis. Ichinohe T, Pang IK, Kumamoto Y, Peaper DR, Ho JH, Murray TS, et al.

Microbiota regulates immune defense against respiratory tract influenza a virus infection. Schuijt TJ, Lankelma JM, Scicluna BP, De Sousa E Melo F, Roelofs JJTH, De Boer JD, et al. The gut microbiota plays a protective role in the host defence against pneumococcal pneumonia.

Felix KM, Jaimez IA, Nguyen TVV, Ma H, Raslan WA, Klinger CN, et al. Gut microbiota contributes to resistance against pneumococcal pneumonia in immunodeficient ragl mice.

Front Cell Infect Microbiol. Davis KL. Low gut microbiota diversity in early infancy precedes asthma at school age.

Sze MA, Dimitriu PA, Hayashi S, Elliott WM, McDonough JE, Gosselink J V. The lung tissue microbiome in chronic obstructive pulmonary disease. Enaud R, Prevel R, Ciarlo E, Beaufils F, Wieërs G, Guery B, et al.

The gut-lung axis in health and respiratory diseases: a place for inter-organ and inter-kingdom crosstalks. Charlson ES, Bittinger K, Haas AR, Fitzgerald AS, Frank I, Yadav A, et al. Topographical continuity of bacterial populations in the healthy human respiratory tract.

Hardy BL, Dickey SW, Plaut RD, Riggins DP, Stibitz S, Otto M, et al. Corynebacterium pseudodiphtheriticum exploits staphylococcus aureus virulence components in a novel polymicrobial defense strategy. Aktas B, Aslim B. Gut-lung axis and dysbiosis in COVID Turkish J Biol. Wang J, Li F, Wei H, Lian Z-X, Sun R, Tian Z.

Respiratory influenza virus infection induces intestinal immune injury via microbiota-mediated Th17 cell—dependent inflammation. Sencio V, Barthelemy A, Tavares LP, Machado MG, Soulard D, Cuinat C, et al.

Gut dysbiosis during influenza contributes to pulmonary pneumococcal superinfection through altered short-chain fatty acid production. Cell Rep. Yasui H, Kiyoshima J, Hori T. Reduction of influenza virus titer and protection against influenza virus infection in infant mice fed lactobacillus casei shirota.

Clin Diagn Lab Immunol. Groeger D, Schiavi E, Grant R, Kurnik-Łucka M, Michalovich D, Williamson R, et al. Intranasal bifidobacterium longum protects against viral-induced lung inflammation and injury in a murine model of lethal influenza infection.

Endam LM, Alromaih S, Gonzalez E, Madrenas J, Cousineau B, Renteria AE, et al. Intranasal application of lactococcus lactis W is safe in chronic rhinosinusitis patients with previous sinus surgery.

Spacova I, Petrova MI, Fremau A, Pollaris L, Vanoirbeek J, Ceuppens JL, et al. Intranasal administration of probiotic Lactobacillus rhamnosus GG prevents birch pollen-induced allergic asthma in a murine model.

Bayarsaihan D. Epigenetic mechanisms in inflammation. J Dent Res. De Brito Oliveira Costa E, Pacheco C. Epigenética: regulação da expressão gênica em nível transcricional e suas implicações. Semin Ciências Biológicas e da Saúde.

Imai K, Ochiai K. Role of histone modification on transcriptional regulation and HIV-1 gene expression: possible mechanisms of periodontal diseases in AIDS progression.

J Oral Sci. Verdin E, Ott M. Nat Rev Mol Cell Biol. Chen J, Zhou Y, Mueller-Steiner S, Chen LF, Kwon H, Yi S, et al. SIRT1 protects against microglia-dependent amyloid-β toxicity through inhibiting NF-κB signaling.

Ito K, Ito M, Elliott WM, Cosio B, Caramori G, Kon OM, et al. Decreased histone deacetylase activity in chronic obstructive pulmonary disease. N Engl J Med. Evans LW, Ferguson BS. Food bioactive HDAC inhibitors in the epigenetic regulation of heart failure.

Kris-Etherton PM, Hecker KD, Bonanome A, Coval SM, Binkoski AE, Hilpert KF, et al. Bioactive compounds in foods: their role in the prevention of cardiovascular disease and cancer. Am J Med. Santos DI, Saraiva JMA, Vicente AA, Moldão-Martins M. Methods for determining bioavailability and bioaccessibility of bioactive compounds and nutrients.

In: Barba FJ, Saraiva JMA, Cravotto G, Lorenzo JM, editors. Innovative Thermal and Non-Thermal Processing, Bioaccessibility and Bioavailability of Nutrients and Bioactive Compounds.

Lisbon: Woodhead Publishing Siriwardhana N, Kalupahana NS, Cekanova M, LeMieux M, Greer B, Moustaid-Moussa N. Modulation of adipose tissue inflammation by bioactive food compounds.

Roy SK, Chen Q, Fu J, Shankar S, Srivastava RK. Resveratrol inhibits growth of orthotopic pancreatic tumors through activation of FOXO transcription factors. Beijers RJHCG, Gosker HR, Schols AMWJ. Resveratrol for patients with chronic obstructive pulmonary disease: hype or hope?

Curr Opin Clin Nutr Metab Care. Koyuncu E, Budayeva HG, Miteva Y V. Sirtuins are evolutionarily conserved viral restriction factors. Tang L, Chen Q, Meng Z, Sun L, Zhu L, Liu J, et al. Suppression of sirtuin-1 increases IL-6 expression by activation of the Akt pathway during allergic asthma.

Cell Physiol Biochem. Ghanim H, Sia CL, Korzeniewski K, Lohano T, Abuaysheh S, Marumganti A, et al. A resveratrol and polyphenol preparation suppresses oxidative and inflammatory stress response to a high-fat, high-carbohydrate meal.

J Clin Endocrinol Metab. Cottart CH, Nivet-Antoine V, Beaudeux JL. Review of recent data on the metabolism, biological effects, and toxicity of resveratrol in humans. Cherneva R V. Epigenetic targets for therapeutic approaches in COPD and asthma.

Nutrigenomics — possible or illusive. Folia Med. Knobloch J, Hag H, Jungck D, Urban K, Koch A. Resveratrol impairs the release of steroid-resistant cytokines from bacterial endotoxin-exposed alveolar macrophages in chronic obstructive pulmonary disease. Basic Clin Pharmacol Toxicol. Balasubramanyam K, Varier RA, Altaf M, Swaminathan V, Siddappa NB, Ranga U, et al.

Yun JM, Jialal I, Devaraj S. Epigenetic regulation of high glucose-induced proinflammatory cytokine production in monocytes by curcumin. Meja KK, Rajendrasozhan S, Adenuga D, Biswas SK, Sundar IK, Spooner G, et al. Curcumin restores corticosteroid function in monocytes exposed to oxidants by maintaining HDAC2.

Xu Y, Liu L. Curcumin alleviates macrophage activation and lung inflammation induced by influenza virus infection through inhibiting the NF-κB signaling pathway. Influenza Other Respi Viruses.

Musial C, Kuban-Jankowska A, Gorska-Ponikowska M. Beneficial properties of green tea catechins. Tabak C, Arts ICW, Smit HA, Heederik D, Kromhout D.

Chronic obstructive pulmonary disease and intake of catechins, flavonols, and flavones: the morgen study. Younes M, Aggett P, Aguilar F, Crebelli R, Dusemund B, Filipič M, et al. Scientific opinion on the safety of green tea catechins. Mao R, Qiu Y, He JS, Tan JY, Li XH, Liang J, et al.

Manifestations and prognosis of gastrointestinal and liver involvement in patients with COVID a systematic review and meta-analysis. Lancet Gastroenterol Hepatol. Wiersinga WJ, Rhodes A, Cheng AC, Peacock SJ, Prescott HC.

Pathophysiology, transmission, diagnosis, and treatment of coronavirus disease COVID : a review. Demir M, Demir F, Aygun H. Vitamin D deficiency is associated with COVID positivity and severity of the disease.

J Med Virol. Infante M, Buoso A, Piere M, Lupissela S, Nuccetteli M, Bernardini S, et al. Low vitamin d status at admission as a risk factor for poor survival in hospitalized patients with COVID an italian retrospective study.

J Am Coll Nutr. Gavioli EM, Miyashita H, Hassaneen O, Siau E. An evaluation of serum hydroxy vitamin D levels in patients with COVID in New York city. Basaran N, Adas M, Gokden Y, Turgut N, Yildirmak T, Guntas G.

The relationship between vitamin D and the severity of COVID Bratisl Lek List. Huang C, Wang Y, Li X, Ren L, Zhao J, Hu Y, et al. Clinical features of patients infected with novel coronavirus in Wuhan, China. Jain SK, Micinski D, Tajesh P. l-Cysteine stimulates the effect of vitamin d on inhibition of oxidative stress, IL-8, and MCP-1 secretion in high glucose treated monocytes.

Cuschieri S, Grech S. At risk population for COVID multimorbidity characteristics of european small island state. Public Health. Codo AC, Davanzo GG, Monteiro L de B, de Souza GF, Muraro SP, Virgilio-da-Silva JV, et al.

Cell Metab. Muhammad Y, Kani YA, Iliya S, Muhammad JB, Binji A, El-Fulaty Ahmad A, et al. Deficiency of antioxidants and increased oxidative stress in COVID patients: a cross-sectional comparative study in jigawa, northwestern Nigeria.

SAGE Open Med. Midha IK, Kumar N, Kumar A, Madan T. Mega doses of retinol: a possible immunomodulation in Covid illness in resource-limited settings. Rev Med Virol. Majeed M, Nagabhushanam K, Gowda S, Mundkur L.

An exploratory study of selenium status in healthy individuals and in patients with COVID in a south Indian population: the case for adequate selenium status.

Clementi N, Scagnolari C, D'Amore A, Palombi F, Criscuolo E, Frasca F, et al. Naringenin is a powerful inhibitor of SARS-CoV-2 infection in vitro. Pharmacol Res. Keywords: nutrients, lung health, pulmonary chronic diseases, asthma, COPD, SARS-CoV-2 infection, COVID Citation: Gozzi-Silva SC, Teixeira FME, Duarte AJS, Sato MN and Oliveira LM Immunomodulatory Role of Nutrients: How Can Pulmonary Dysfunctions Improve?

Received: 01 March ; Accepted: 02 August ; Published: 07 September Copyright © Gozzi-Silva, Teixeira, Duarte, Sato and Oliveira. This is an open-access article distributed under the terms of the Creative Commons Attribution License CC BY.

The use, distribution or reproduction in other forums is permitted, provided the original author s and the copyright owner s are credited and that the original publication in this journal is cited, in accordance with accepted academic practice.

No use, distribution or reproduction is permitted which does not comply with these terms. mendonca usp. Nutrition, Immunity and Lung Health: Time to Take Center Stage. Beetroot and beet greens have been shown to benefit lung function, relax blood pressure and optimize oxygen intake, all of which can help someone struggling to breathe.

Beets are also packed with vitamins and nutrients that promote lung health, like magnesium and potassium. Pumpkins are rich in carotenoids, which are associated with higher lung function. Carotenoids also contain antioxidant and anti-inflammatory properties, which promote overall health and comfort.

Tomatoes are one of the richest vegetable sources of lycopene, a carotenoid that has been associated with improved lung function. Consuming tomatoes and tomato products has also been linked to reduced lung decline and airway inflammation.

Leafy greens such as bok choy, spinach and kale are a rich source of carotenoids, iron, potassium, calcium and vitamins. These nutrients have anti-inflammatory and antioxidant effects, which can help reduce lung inflammation and promote overall health.

Sodium causes fluid retention, which can lead to shortness of breath in patients who have lung disease. And while the salt shaker is the most obvious source of sodium, the bulk of sodium intake is actually already in the food. To reduce salt intake: Opt for herbs and spices to season food and check food labels before purchasing.

As the body digests dairy products, a breakdown of milk digestion called casomorphin increases the amount of phlegm and mucus produced by the body.

This can increase coughing, which can cause wheezing and pain in COPD patients. Cured meats and cold cuts contain nitrates, which companies often add to these products for color and to help extend shelf life. These nitrates, however, have been found to lead to an increase in COPD-related hospital readmissions.

Drinking soda can be harmful to those with lung disease in several ways. First, soda contains carbon dioxide to make it carbonated, which can cause gas and bloating that makes it harder to breathe.

In addition, the high sugar content can increase inflammation and lead to weight gain, both of which can exacerbate COPD symptoms.

To reduce soda intake: Try switching soda out with other noncarbonated, flavored beverages like tea, flavored water or natural juice. Fried foods such as french fries and onion rings contain unhealthy fats that can cause bloating and discomfort by pushing on the diaphragm.

In addition to lung discomfort caused by bloating, fried foods over time can lead to higher cholesterol and weight gain. For people living with lung disease, these things can worsen symptoms. Simple carbohydrates such as white bread should be avoided, as it takes more work for the lungs to metabolize them.

Switching out these simple carbs for whole-grain, complex carbohydrates can improve lung health. Potato chips are filled with salt and saturated fat, two things that are detrimental to lung health. Trans and saturated fats harm your cardiovascular health and can raise blood pressure.

The salt in chips can also increase water retention, making it harder to breathe. First and foremost, chocolate contains caffeine, which can interfere with medication or increase heart rate. Chocolate is also high in sugar and low in nutrients, making it a generally bad choice for someone with lung disease.

In general, alcohol can increase inflammation in the lungs. The nitrates in processed cold cuts have been linked to lung decline and worsening COPD symptoms. Lean meats like salmon and chicken are a better choice for those who want to eat meat. Lung disease and discomfort are hard to live with.

Keeping your body healthy through diet and nutrition is another way you can improve your overall health and make cancer treatment easier.

To talk about a diet plan while navigating treatment, find a doctor who is right for you. However, as required by the new California Consumer Privacy Act CCPA , you may record your preference to view or remove your personal information by completing the form below. The information on this website is proprietary and protected.

It is not a substitute for professional medical advice, diagnosis or treatment. Any unauthorized or illegal use, copying or dissemination will be prosecuted.

Please read our privacy policy and disclaimer for more information about our website. com is sponsored by law firms.

This website and its content may be deemed attorney advertising. Prior results do not predict a similar outcome. For more information, visit our sponsors page.

The Mesothelioma Center's claim as the most trusted mesothelioma resource is based on our more than 5-star Google and BBB reviews. Our organization also helps more than half of all mesothelioma patients annually diagnosed. We will help you find the best mesothelioma doctor in your area. Our Patient Advocates have relationships with top doctors and cancer centers and can help you schedule and expedite appointments.

Your web browser is no longer supported by Microsoft. Update your browser for more security, speed and compatibility. If you are looking for mesothelioma support, please contact our Patient Advocates at Menu Search. Mesothelioma Diagnosis Pleural Mesothelioma Peritoneal Mesothelioma Epithelioid Mesothelioma Sarcomatoid Mesothelioma Stages Prognosis Symptoms.

Statistics Causes Asbestos Asbestos Cancer Lung Cancer Veterans VA Claims. Treatment Top Mesothelioma Doctors Find a Treatment Center Surgery Chemotherapy Radiation Multimodal Therapy Immunotherapy Clinical Trials.

Chronic obstructive pulmonary disease COPD There is growing evidence that some elements of the diet may benefit lung function or improve COPD symptoms. Cystic Fibrosis Researchers have found that under-nutrition can play a key role in cystic fibrosis CF. Lung infections Deaths among people who are severely malnourished are often due to pneumonia and a low level of vitamin D is a recognised risk factor for the development of respiratory infections.

Pulmonary embolism People who are obese have an increased risk of pulmonary embolism, in which clots block one or more blood vessels in the lung.

Top tips for healthy lungs. Although the effects of diet need further study, it is clear that the following can help to maintain good lung health: High intake of fruit, vegetables and fish Low salt intake Restricted intake of trans-fats and omega-6 fatty acids Maintenance of a body mass index BMI between 21 and 30 Moderate exercise Eating foods rich in antioxidants Eating foods rich in magnesium, such as nuts, cereals, seeds, carrots, spinach and seafood Eating oily fish, shellfish, soy and leafy vegetables to ensure intake of essential omega-3 fatty acid.

Lung conditions Learn about the conditions that can affect our lungs and access our lung condition specific information. Read more. Living with a lung condition Learn more about life with a lung condition and things you can do to improve your quality of life.

Keeping lungs healthy Learn about the factors that can cause lung disease and the ways to reduce your contact with them. Get involved We work hard to involve patients and the public in research, have your say.

News Read clear, short summaries of the most up-to-date research in lung health. Join our mailing list Sign up to get the latest information and research on lung conditions, hear about our upcoming events and campaigns, plus views from experts and patients!

This field is for validation purposes and should be left unchanged. We use cookies on our website to give you the most relevant experience by remembering your preferences and repeat visits. However you may visit Cookie Settings to provide a controlled consent.

Cookie settings ACCEPT REJECT. Close Privacy Overview This website uses cookies to improve your experience while you navigate through the website.

Out of these cookies, the cookies that are categorized as necessary are stored on your browser as they are essential for the working of basic functionalities of the website.

We also use third-party cookies that help us analyze and understand how you use this website. These cookies will be stored in your browser only with your consent. You also have the option to opt-out of these cookies. But opting out of some of these cookies may have an effect on your browsing experience.

Necessary Necessary.

While Dr. Brigham counsels patients on ways to reduce their own exposure, she and others are also looking for ways to reduce risk in those who cannot.

Creative and scalable solutions are urgently needed. Brigham and her team are investigating an intervention that holds promise as both a treatment and as preventative medicine: anti-inflammatory and antioxidant foods. For example, kale, spinach, tomatoes and many other vegetables have high levels of antioxidants like lutein, which helps the body regulate the oxidative stress caused by air pollution.

They also have high levels of fibre, which can stimulate the production of potent inflammation-fighting molecules by the bacteria that live in the gut. Fatty fish like salmon, meanwhile, are packed with omega-3 fatty acids that help to regulate inflammation. Diets with more of these beneficial nutrients — and less of the pro-inflammatory nutrients found in fast foods and processed foods — could help the body to combat the negative effects of air pollution.

Brigham and her team are working with a registered dietician and a healthy food delivery service to measure the possible benefits.

Their study, currently under review, will deliver specially selected meals and groceries to study participants and track how they respond to air pollution exposure.

The diet could be particularly beneficial to communities that are disproportionately affected by air pollution and respiratory illness.

ILC2s play a key role in maintaining the epithelial barrier of the respiratory tract, through the production of cytokines including IL-4, IL-5, IL-9, IL, and the epidermal growth factor-like molecule amphiregulin It was demonstrated in the lung that the depletion of ILC2 negatively affected the integrity of the epithelial barrier of the airways after infection by the influenza virus.

This is because the depletion of ILC2 caused a failure to generate hyperplastic epithelial cells, leading to the deterioration of the epithelial lining In the lung, IL is produced especially by ILC3 and has also been shown to be involved in maintaining epithelial barrier function, mucus production, and tissue repair.

Thus, ILCs contribute to barrier surveillance and epithelial protection and repair through coordinated interactions with other cells in the lung In patients with COPD, the signatures of IL and the accumulation of ILC1s are elevated. IL induces the conversion of ILC2s into interferon IFN -γ-producing ILC1s, thus contributing to the type 1 inflammatory lesion associated with COPD In addition to effector cells, the airway mucosa also has bronchial-associated lymphoid tissue BALT , which comprises aggregates of lymphoid cells underlying Peyer's plaques.

The presence of BALT is common in young children; however, its importance in adult humans has been questioned. It has been suggested that BALT may play a significant role in local immune homeostasis within the respiratory tract early in life, when important elements within central lymphoid structures are not fully mature 6 , Part of BALT role is related to the humoral immune response of the mucosa and more specifically to the production of immunoglobulin Ig A IgA IgA is the antibody isotype most present in the mucosal immune system and consists of its main defense mechanism.

Provide the first line of defense in these locations against external agents without inducing a potentially harmful inflammatory response In the infection context, sIgA helps protect the mucosal epithelium barrier through two main protective functions The first, called immune exclusion, acts on the stromal epithelial portion, where IgA can form complexes with antigens.

These immune complexes can be captured by phagocytic cells, absorbed into the vascular system or transported through the epithelium to the lumen. This immune elimination feature of IgA allows the maintenance of mucous tissues and protects against excess antigens that can cause infections The second function is based on intracellular neutralization In this case, IgA is able to prevent the assembly of the virus and neutralizes viral replication.

Thus, it can interfere with the ability of antigens to adhere and penetrate the mucosa SIgA deficiency was demonstrated on the bronchial mucosa surface of ex-smokers with COPD. The deficiency was associated with latent or persistent herpesvirus infection, thickening of the submucosa and fibrotic remodeling of the airway walls Associated epithelial damage also supports an inefficient first line of defense with decreased mucociliary clearance and IgA secretion On the other hand, in asthma it is believed that the activation of granulocytes represents a driving force, since Fc alpha receptor FcαR is widely distributed in granulocytes.

These cells secrete amines, for example, serotonin, and peptides, for example, bombesin. PNECs play a role in the growth and differentiation of lung cells, while NEBs degranulate in the presence of hypoxia, acting as hypoxia-sensitive chemoreceptors 3.

Immune cells and their organization in the lung are illustrated in Figure 1. Figure 1. Pulmonary immunity overview. Lungs are in constant contact with many suspended substances, which are relatively harmless, such as pollutants, microbiota, and allergens. A Ciliated pseudostratified columnar epithelium covers all respiratory tract, providing a pathway for movement and conditioning of the air entering the lungs, as well as, controls the actions of the mucociliary escalator directing the particles to outside the lung.

In association, Goblet cells produce mucins to create a protective layer of mucus, forming a first barrier of defense. Airway fluids also contain antimicrobial peptides AMP , defensins, cytokines, and antibodies, mainly secretory IgA.

To ensure the homeostasis, in the lamina propria, immune cells act both to identify and respond to sterile threats and to control the inflammatory process, preventing that inflammation from compromising lung function.

In addition, follicular regions rich in T and B lymphocytes BALT—bronchus-associated lymphoid tissue play a crucial role in fighting against infections. B Alveolus are in broadly interaction with the external environment, where lung cells secrete surfactants proteins and alveolar macrophages are highly phagocytic.

Although the lungs have mainly respiratory functions, there are descriptions of their role in non-respiratory processes. The lung has a very stretchable vasculature, which allows it to deal with variations in venous return, especially during postural changes, exercises and increased intravascular volume.

When there is an increase in cardiac output, underperfused areas of the pulmonary vasculature are recruited to accommodate the increase in blood flow and prevent an increase in pulmonary arterial pressures 3. The pulmonary endothelium is also a source of fibrinolysin activator, which converts plasminogen to fibrinolysin.

The lung, therefore, has an efficient fibrinolytic system, capable of smoothing clots in the pulmonary circulation In addition, the lungs are also an essential site for the degradation and inactivation of chemical mediators, playing a role in the biotransformation and detoxification of inhaled substances 3.

The lungs express enzymes related to the metabolism of xenobiotics, the main enzymes being involved in the cytochrome P family and participating in oxidative metabolism, as well as in the metabolic bioactivation of many organic toxins, including pro-carcinogens An important role of the lungs can therefore be to act as a buffer binding to xenobiotics, preventing an acute increase in systemic concentrations, as well as playing a role in the biotransformation of inhaled substances All these data showed the complexity of the mechanisms and interactions between immune cells, pulmonary epithelium cells and external agents microbiota, innocuous agents, pathogens , for the maintenance of lung health and its respiratory activity.

Homeostasis can be defined as the stability of a complex system via internal mechanisms of self-regulation resilient to external disturbances Considering that the lungs are chronically exposed to various pathogenic or non-pathogenic environmental antigens, maintaining a network of cells residing in the tissue that continuously monitors the external environment and instructs tolerance to innocuous inhaled particles is of paramount importance to ensure pulmonary homeostasis 6.

In this sense, diet and nutrition are becoming increasingly recognized as modifiable contributors to lung health, thus being a central parameter that governs the systemic immune system, homeostasis and pulmonary inflammation. Different dietary components can have direct effects on lung health or be used as sources of energy for immune function.

In fact, their resulting metabolites can be potent immune modulators COPD is a common respiratory disease characterized by functional and structural changes generated, especially, by inhaling harmful particles It has been considered a disease due to the chronic inflammation leading to remodeling of the extracellular matrix, in which the extent of the inflammation is related to the degree of airflow obstruction In addition to inflammation, the imbalance between proteases and antiproteases and oxidative stress are processes involved in the pathogenesis of COPD The activation of PRRs by damage-associated molecular patterns DAMPs , which are released after tissue damage, results in the synthesis of inflammatory cytokines.

One of the possible mechanisms of cytokine production involved in the pathogenesis of COPD is dependent on caspase 1 and the formation of the P3 inflammasome of the nucleotide-binding oligomerization domain NLR The NLRP3 inflammasome leads to the secretion of IL-1β and IL, which activate neutrophils, macrophages, Th1 and Th17 lymphocytes, leading to inflammation of the airways Neutrophils are strongly involved in inflammation, and high levels of sputum neutrophils are associated with the severity of COPD In addition, the reduced phagocytic function of macrophages influences the reduction of neutrophil apoptosis, which can generate secondary necrosis The oxidative load is also increased in COPD.

The release of reactive oxygen and nitrogen species released by inflammatory cells promotes oxidative stress, which may lead to inactivation of antiproteases or stimulation of mucus production.

It can also increase the activation of transcription factors such as nuclear factor κB and therefore, the gene expression of proinflammatory mediators Another inflammatory respiratory disease is asthma, which is a common chronic airway disorder characterized by variable and recurrent symptoms, airflow obstruction, bronchial hyperresponsiveness and underlying inflammation.

Atopy, or the genetic predisposition to develop specific IgE antibodies against environmental allergens, is the strongest risk factor for the development of asthma. Although asthma has been viewed as a reversible disease, evidence indicates that permanent structural changes in the airway are typically seen and include subbasement membrane fibrosis, smooth muscle hyperplasia, new vessel formation, and glandular hyperplasia In this context, long-term asthma is associated with an accelerated decline in lung function.

Although lower than that observed in individuals with COPD, it is also an indication of structural and possibly permanent changes in the airways The inflammatory response in the airways of patients with asthma involves an interaction of the respiratory epithelium, innate immune system and adaptive immunity that initiates and leads to a chronic inflammatory response Prospective analyses since birth show that most asthma development occurs in early childhood and has an allergic component.

Individuals with allergic asthma have eosinophilic inflammation in the lungs, as well as increased mediators related to the adaptive response of the Th2 subset, such as IL-4, IL-5 and IL, and serum IgE elevation.

The Th17 subset may also play a role in asthma by mediating neutrophilic inflammation The decrease in the suppressive activity of Treg cells IL and TGF-β-producing cells represents additional mechanisms that contribute to asthma, perhaps partly distorting the system toward an increased Th2 response Although respiratory diseases extend throughout the course of life, the onset of asthma occurs in childhood, while COPD is commonly associated with groups in advanced age.

In addition, there are significant changes in immunity associated with aging, with an increased risk of lung disease in the elderly The respiratory tract is constantly exposed to the external environment and must be prepared to respond to pathogens. Although an effective immune response to eliminate viral pathogens is essential, a prolonged or exacerbated response can cause damage to the respiratory tract.

Thus, the antiviral immune response represents a balancing act between virus elimination and immune-mediated lung injury Respiratory epithelial cells are usually the first cell type to be infected. The PRRs expressed in these cells recognize viral pathogen-associated molecular patterns PAMPs triggering the production and release of type I and III interferons and other proinflammatory mediators, such as cytokines, chemokines and antimicrobial peptides, which initiate the innate and adaptive immune response.

Thus, the degree of activation of PRR influences the degree of recruitment of immune cells and release of proinflammatory mediators and, subsequently, any resulting immunopathology Type I IFNs also directly promote lymphocyte functional activity by stimulating IFN-γ secretion, which in turn activates macrophages and phagocytosis, increases the presentation of antigens through DCs and limits viral replication.

Type I IFNs also increase the cytotoxic activity of T cells and Natural Killer NK cells and promote the humoral response As a consequence of widespread effects on host immune responses, IFNs can facilitate inflammation and injury to the lungs in an indirect manner during acute viral infection Diet and nutrition can be important, modifiable, risk factors for the development, progression and management of obstructive pulmonary diseases, such as asthma, COPD, and pulmonary viral infections.

Dietary factors with a potential protective role in the oxidative process and inflammatory response have been implicated in the genesis, evolution or protection against these diseases Below, the main nutrients that can influence homeostasis and lung diseases are described Figure 2.

In addition, immunomodulatory role of nutrients in these pulmonary diseases are exemplified in Table 1. Figure 2. Immunomodulatory properties of nutrients in lungs. Nutrients are able to ameliorate the development and severity of pulmonary diseases, since they can act on several immune cells and modulate immune response in inflammatory processes.

In this context, minerals, flavonoids, vitamins, and fatty acids reduce the expression of inflammatory mediators such as cytokines and chemokines , as well as, have antioxidant effect, decreasing the deleterious effects of asthma and chronic obstructive pulmonary disease COPD in the lungs.

In addition, fibers and fatty acids also can modulate intestinal microbiota, which contribute to lung homeostasis through gut-lung axis.

Regarding pulmonary viral infections, vitamins, and flavonoids are the main dietary components with antiviral action. Table 1. Immunomodulatory proprieties of nutrients in lung inflammatory diseases.

Vitamins are micronutrients available in several kinds of foods and can be of animal or vegetable origin. In addition to their nutritional role, they also participate in immunity and homeostasis of the mucosa, such as the intestinal and pulmonary mucosa.

Regarding lung health and homeostasis, vitamins A, C, and D can be considered the most important, not only for their anti-inflammatory action but also for participating in the immune response against pathogens, as we describe below. Several studies on vitamin A have shown that the active metabolite retinoic acid RA has a fundamental role in the maintenance and modulation of the immune response and the homeostasis of epithelial tissues and mucosa and is important in the control of inflammatory diseases In clinical studies, vitamin A deficiency can be correlated with asthma, since serum retinoid concentrations are significantly lower in patients with asthma than in healthy control subjects, mainly in patients with severe asthma 99 , In an experimental asthma model, vitamin A deficiency in mice also worsened the inflammatory condition by increasing the Th2 cytokines IL-5 and IL and pulmonary inflammation However, the administration of RA increases Treg cells in the lungs, attenuating inflammation Supplementation with RA also promotes downregulation of the GATA3 and RORγt transcription factors, inhibiting Th2 and Th17 cytokines in the lungs 64 highlighting the importance of adequate intake of vitamin A for asthma.

Vitamin A also plays an important role in the humoral response and antiviral mechanisms of the immune response. For example, RA is essential to the production of IgA antibodies and RA deficiency associated with zinc deficiency leads to a decrease in serum IgA, promoting damage to humoral immunity Moreover, RA demonstrated the ability to decrease the viral load of Morbillivirus in infected mice This decrease was possible due to the mechanism that induces RIG-1 expression, promoting the production of type I IFNs by increasing the recognition of viral dsRNA by immune cells.

Another study showed that treatment with retinol or RA in mice infected with acute gastroenteritis virus Norovirus increased the production of IFN-β, inhibiting norovirus replication In the context of obesity, vitamin A supplementation significantly improved vitamin A levels in the lungs of diet-induced obese mice, decreased inflammatory cytokines in the blood and improved antibody responses after vaccination against the influenza A H1N1 virus, thereby promoting a reduction in viral loads post challenge These data suggest that vitamin A has a strong impact on the vaccine response.

Vitamin C is another important micronutrient for the immune response in the lungs. A trial study with elderly patients with pneumonia has shown that treatment with two doses of vitamin C was able to reduce severity and mortality Moreover, another antiviral effect of vitamin C could be seen in a study with H1N1-infected mice.

In this study, supplementation with vitamin C increased IFN-γ production by NK cells and reduced the viral infection and lung inflammation induced by H1N1 infection Similar results have been shown in peripheral blood mononuclear cell PBMC culture with increases in CD25 and CD69 expression in T and NK cells, promoting the activation of the cellular antiviral response Vitamin D is important for lung health since birth, even in the absence of infections.

A recent study showed a correlation between vitamin D deficiency and respiratory distress syndrome in premature infants RDS In this same study, it was also shown that patients with higher 25 OH D levels can be preventive for the development of RDS.

RDS presents as the main characteristic of pathological surfactant deficiency and pulmonary immaturity, demonstrating the role of vitamin D in promoting lung maturity. Vitamin D also has great potential in modulating the immune response against respiratory viruses For example, vitamin D regulates the expression of antimicrobial peptides LL and β-defensin 2 , , both with antiviral activity against respiratory syncytial virus RSV 84 , These antimicrobial peptides block viral cellular entry, inhibiting the production of new infectious particles and consequently, diminishing the spread of infection, and virus-induced epithelial cell death The antiviral effect of vitamin D was also described in RSV infection in the first year of life, since vitamin D deficiency has a positive correlation with RSV infection In addition to antiviral effects, vitamin D also presents anti-inflammatory effects during viral infections.

In vitro studies with primary human tracheobronchial epithelium hTBE pretreated with the active form of vitamin D, 1,dihydroxycholecalciferol [1,25 OH 2], showed less proinflammatory cytokine production after RSV infections due to high levels of the NF-κB inhibitor IκBα and IκBα induced by vitamin D pretreatment without affecting the antiviral response Similar results have been shown in a treated human alveolar epithelial-cell line with 1,25 OH 2 D3 before or after influenza A H1N1 exposure, with a decrease in proinflammatory cytokines and virus-induced cell death but without an effect on viral clearance The anti-inflammatory effect of vitamin D can also be seen in COPD patients.

Recently, it has been shown that COPD patients present low serum levels of 25 OH D and high serum levels of proinflammatory cytokines compared to healthy individuals. Vitamin D deficiency was more robust in patients with grade 4 COPD These patients also presented NF-κB and activator protein 1 AP-1 signaling activation and a decrease in the NF-κB inhibitor IκBα and IκBα.

All these data showed the importance of vitamin D in controlling this inflammation. Regarding vitamin E, there are few reports that describe its immunoregulatory role in the lungs; however, in a recent study with an experimental model of asthma and allergic rhinitis, it was demonstrated that vitamin E reduced the symptoms of the pathology due to its anti-inflammatory action In this study, mice treated with vitamin E showed improvement in the pulmonary inflammatory condition, with a decrease in the presence of serum Th2 cytokines and in bronchoalveolar lavage; in addition to a decrease in constriction and mucus secretion in the mice, especially in combination with selenium.

Together, these data show the importance of adequate consumption of vitamins for the maintenance of lung health. Minerals are inorganic substances present in food, such as magnesium, selenium, and zinc, that play an important role in cellular metabolism and the immune response. Dietary magnesium has shown beneficial bronchodilator effects in asthma as well as in severe asthma exacerbations, and a single dose of intravenous magnesium sulfate MgSO 4 was able to reduce hospitalizations and improve lung function On the other hand, the deficiency in magnesium consumption in asthmatic individuals was related to negative actions in the bronchial smooth muscle 12 , However, it was also described in a clinical trial with asthmatic individuals that supplementation with magnesium administered together with vitamin C did not demonstrate any clinical benefit in lung function, symptoms or the possibility of decreasing the dose of steroids Selenium acts as an antioxidant and, when interacting with other nutrients, such as vitamin E, protects cells against oxidative stress.

Selenium is an essential component of the enzyme glutathione peroxidase GSH-Px , which reduces hydrogen peroxide and other organic peroxides to harmless substances.

By detoxifying peroxides, GSH-Px prevents peroxidation and subsequent instability of cell membranes. It has been proposed that selenium, as a component of GSH-Px, can protect membranes in asthmatic airways from peroxide-induced damage In this context, previous studies have shown that peripheral blood and platelet GSH-Px activity is reduced in sensitive asthmatic patients and case-control studies have reported lower levels of selenium in the blood of individuals with asthma compared to controls, with selenium being negatively associated with asthma , However, a study with children did not find a relationship between the levels or intake of selenium and results related to asthma Studies with adult asthmatic subjects who were on inhaled-steroid use for 24 weeks did not reveal any clinical benefit from selenium supplementation , Zinc is essential for the synthesis of DNA and is an enzymatic cofactor that participates in various physiological and metabolic functions in the body.

It is also known to induce the production of metallothionein, which is rich in cysteine and is, therefore, a potent OH-radical scavenger In relation to control subjects, a study showed that COPD patients had lower serum zinc concentrations, and this reduction was even more pronounced in patients with COPD grade III severe COPD compared to those with milder disease grades I and II Low plasma zinc content has been associated with respiratory tract infections in children, while zinc supplementation has been associated with a reduction in the incidence of pneumonia in children without vitamin A deficiency 13 , Zinc supplementation improves immune functions, including reduced skin hypersensitivity and an increased number of TCD4 cells 87 , The altered proportion of Th1 and Th2 cells in favor of allergic reactions induced by Th2 cells is a consequence of zinc deficiency; therefore, zinc plays an important role in the proper differentiation of T cells.

In addition, tolerogenic immunoreaction is triggered by changes in intracellular zinc levels due to the induction of Treg cells and the damping of proinflammatory Th17 and Th9 cells In experimental models, zinc deficiency has been shown to impair cellular and humoral immune function , , whereas, the zinc transporter 10 ZIP10 is necessary for adequate antibody responses after B-cell receptor BCR activation In the context of viral infections, it has been reported that zinc is able to inhibit the RNA polymerase necessary for the replication of RNA viruses, indicating that zinc may play an essential role in the defense of the host against RNA viruses The replication of influenza virus was inhibited in vitro by the zinc ionophore pyrrolidine dithiocarbamate In mechanistic terms, the strong correlation between homeostatic iron concentrations and the presence of oxygen in the lungs is evident, where both systems must be adequately controlled for full lung function.

Oxygen to be transported efficiently by erythrocytes depends on the presence of hemoglobin, a protein capable of binding oxygen through its central iron atom In addition to participation in hemoglobin synthesis, iron is of great importance for other essential metabolic processes, such as DNA repair, transcription and energy production in mitochondria.

However, free iron is highly reactive and potentially toxic and is able to catalyze the production of reactive oxygen species ROS and damage lipids, nucleic acids, and proteins, causing tissue damage For this reason, iron is mostly linked to protein groups to neutralize its reactivity.

Therefore, like any other cell, lung cells must acquire adequate amounts of iron to supply metabolic needs and to ensure lung function and survival. In parallel, lung cells must avoid excess iron, oxidative stress and resulting injuries that can impair lung function Growing evidence suggests that natural polyphenols, particularly flavonoids, can ameliorate the inflammatory process Flavonoids are polyphenolic compounds broadly present in plants According to their structures and the hydroxylation and glycosylation patterns of benzene rings, flavonoids can be present in different subclasses, which include flavanols, flavanones, flavones, isoflavones, flavonols, and anthocyanidins These bioactive compounds are particularly abundant in the human diet of fruits, vegetables, tea, red wine, chocolate, and coffee However, their considerable structural diversity and in vivo bioavailability allow them to modulate different signaling pathways The immunomodulatory properties of flavonoids are associated with the inhibition of protein kinases, enzymes involved in arachidonic acid metabolism and the regulation of key signaling pathways, such as NF-κB and nuclear-related factor 2 Nrf2 — Additionally, they have antioxidant effects due to their scavenging activity for reactive oxygen or nitrogen species and by a reduction in oxidative stress , Some flavonoids also exert anti-inflammatory effects by blocking the NLRP3 inflammasome, inhibiting proinflammatory cytokine production, and downregulating chemokines — Flavonoids are reported to possess a wide variety of biological activities on immune cells, modulating their activation, differentiation and proliferation, and they can act on neutrophils, T cells, NK cells, DCs, and macrophages by reducing the expression of proteins and receptors 69 , 70 , In this context, eosinophils, neutrophils, mast cells and basophils are also affected by flavonoids, which inhibit degranulation and decrease the release of histamine and other mediators 71 , 72 , In addition, the improvement of the immune response is associated with antibody production, cytotoxic activity, and enhancement in regulatory T cells Some studies point to the antiviral properties of flavonoids against a wide range of DNA and RNA viruses.

For example, apigenin flavone is active against picornavirus RNA virus , inhibiting viral activity 92 ; catechin flavanol reduces the replication cycle of the hepatitis B virus, herpes simplex and adenovirus 93 ; naringenin flavanone has antiviral activity against dengue, Zika, hepatitis C, chikungunya, yellow fever, and human immunodeficiency virus In addition, flavonoids were found to reduce lung injury and the inflammatory response during influenza H1N1 infection in a mouse model Recently, flavonoids have also been proposed against coronavirus infection 69 , There are strong evidences that concerns the role of flavonoids in several pulmonary diseases through decreased release of inflammatory mediators, fibrotic factors, and edema, and the attenuation of Th17 inflammation and suppression of airway hyperresponsiveness 69 , 72 , Furthermore, flavonoid supplementation is also effective in reducing the incidence of upper respiratory tract infections In general, chronic diseases are caused by chronic inflammation; therefore, flavonoids have been proposed as potentially useful treatments for inflammatory diseases.

Dietary fibers are defined as the edible parts of plants or analogous carbohydrates. They are resistant to digestion and absorption in the human small intestine and are completely or partially fermented in the large intestine. Dietary fiber includes polysaccharides, oligosaccharides, lignin and associated plant substances.

Studies indicate that fiber intake can reduce the risk of COPD due its anti-inflammatory effect, since systemic inflammation is an important feature of COPD Increased dietary fiber intake has been linked to reduced systemic inflammation and C-reactive protein CRP levels Considering that CRP is a marker of systemic inflammation activated by the innate immune system and a possible molecule associated with vascular disease , it is possible that its action is related to lung damage.

Dietary fibers can also modify the intestinal microbiota, especially interfering with the ratio between Firmicutes and Bacteroidetes. As a result, there is an increase in short-chain fatty acids that are derived from the fermentation of dietary fibers.

These fatty acids have relevant protection in the regulation of neutrophils, lung function and COPD, and epithelial protection against infection Most of the lipid mediators that regulate inflammation are metabolites from omega-6 ω-6 or omega-3 ω-3 fatty acids, including arachidonic acid, linoleic acid, eicosapentaenoic acid and docosahexaenoic acid.

ω-3 and ω-6 are considered essential fatty acids, as the body is not able to produce them, and their acquisition through diet is necessary Most vegetable oils are significant sources of ω-6, while cold-water marine fish are the main sources of ω-3 Generally, ω-6 fatty acids are proinflammatory, and ω-3 fatty acids are anti-inflammatory Epidemiological data describe that populations with a higher intake of ω-6 fatty acids have a higher prevalence of asthma in relation to those that consume smaller amounts of ω-6 and with a higher intake of ω-3 fatty acids, considering that ω-3 produces ecosystems that are less proinflammatory than those derived from ω-6 , Food supplementation with fish oil rich in ω-3 fatty acids for 10 months was able to reduce asthma scores and increase acetylcholine thresholds in children with bronchial asthma In other studies, the administration of fish oil prevented only allergen-induced late asthmatic reactions and had no effect on immediate reactions In a murine model, ω-3 supplementation improved survival, reduced bacterial invasion into the blood and lungs, and decreased overall lung tissue inflammation and cell death compared to ωsupplemented diets Another fatty acid described in lung protection is short-chain fatty acids SCFAs.

SCFAs are derived from the fermentation of fibers by means of intestinal bacteria and are essential to regulate a wide variety of processes in the gastrointestinal tract, but they are also potent mediators of the function, maturation, and destiny of immune cells Oral application of SCFAs to mice during pregnancy and weaning protected the offspring from allergic lung inflammation, potentially inducing Tregs in the offspring's lungs SCFAs such as acetate and butyrate, in addition to their anti-inflammatory activity , also play an important role in infectious diseases.

Galvão et al. showed that the absence of the receptor for acetate GPR43 increased susceptibility to Klebsiella pneumoniae infection, with uncontrolled proliferation of bacteria and an inflammatory response. On the other hand, treatment with acetate was efficient for protection during bacterial lung infection Against RSV infection, acetate also protects host mice through GPR43 via another mechanism.

In RSV infection, the antiviral effect is caused by increasing the expression of interferon-stimulated genes in the lungs, leading to the production of IFN-β cytokine In a murine model, it was also seen that SCFAs were able to promote the recruitment of neutrophils into the airways and to protect against infection from the influenza virus The microbiota is a constituted by the microbial commensal communities includes bacteria, fungi, viruses and protozoa that reside in different tissues, especially in gut Its functions range from breaking down complex dietary polysaccharides to competing with pathogens and modulating the mucosa and the development of the immune system, both locally and systematically , However, some studies demonstrate that the nutritional status, since childhood, impacts not only in the immune response and homeostasis but also in the intestinal microbiota, evidencing another way in which nutrition can impact mucosal immunity Regarding pulmonary health and maintenance of homeostasis, experimental evidence has highlighted a cross between the intestinal microbiota and the lungs, called the intestine-lung axis 5.

Thus, the intestinal microbiota, influenced by nutrition, plays an important role in the immune responses developed during infections and inflammatory lung diseases. Below we will describe some aspects regarding the intestine-lung axis in two subsections: gut and airway microbiota.

With a bacterial load on the order of 10 14 bacteria the intestine is the most densely colonized surface of the human body, home to between , and billion bacteria per ml of luminal content The microorganisms present in the intestinal microbiota act as a source of PAMPs that, when recognized by PRRs as TLRs, are in direct contact with the intestinal lumen and promote the proliferation of epithelial cells, expression of antimicrobial peptides and secretion of IgA In addition, the gut microbiota can influence host immunity by inducing the release of anti-inflammatory IL , and proinflammatory IFN-γ, IL, IL-6, and IL cytokines , releasing metabolites — , and controlling the function of phagocytes, including DCs The diversity of the intestinal microbiome has genetically determined variations, but it is also influenced by environmental factors, such as lifestyle and diet For example, variations in the intake of resistant starch or non-starch polysaccharides have been reported to alter specific bacterial-rate levels, such as Ruminococcus bromii and Eubacterium rectal , just as the composition of the intestinal microbiota in breastfed babies superior bifidobacteria, lactobacilli, staphylococci, and streptococci differs considerably from formula-fed babies Bacteroides, Clostridia , and Proteobacteria Regarding obesity, the high consumption of ultra-processed foods, in addition to causing a state of micronutrient deficiencies, may be related to dysbiosis, demonstrating the importance of diet in maintaining a healthy microbiota Dysbiosis in gut microbiota can impair immune responses and pulmonary homeostasis.

In this context, studies in germ-free and antibiotic-treated mice have contributed to the understanding of the relationship between intestinal microbiota and local and systemic homeostasis Fecal transplantation in these animals, thereby reconstituting their microbiota, was able to restore intestinal immunity, influence the development of the mucosal systemic immune system and protect against bacterial and viral infections An experimental model of dysbiosis induced by antibiotic ingestion decreased effector and memory T cell populations in mice infected by Mycobacterium tuberculosis , since dysbiosis affected the activation of innate receptor macrophage inducible C-type lectin mincle of lung DCs.

After the microbiota is restored, DC's ability to activate T cells is also restored. In addition, dysbiosis present in obesity can also be related to changes in the immune response during lung infections On the other hand, promote a healthy gut microbiota is important against pulmonary infections.

Study with microbiota transplantation in gut microbiota-depleted mice infected intranasally with S. pneumoniae , showed that microbiota was able to control bacterial dissemination and inflammation The transplantation of isolated group of host-adapted commensal organisms, such as Segmented filamentous bacteria SFB , also play an important role in lung infections without the need for transplantation of all components of the gut microbiota.

pneumoniae showed that the transplantation of SFB influenced lung protection, not for controlling bacterial infection, but for regulating innate immunity In this study, the SFB promoted a shift in lung neutrophil phenotype from inflammatory neutrophils to pro-resolution neutrophils with low CD18 and high CD62L reducing, this way, the severe tissue damage caused by inflammatory neutrophils.

So, the gut microbiota can also act by decreasing the inflammatory response, reducing the tissue damage caused by the immune response. Besides that, epidemiological studies have described a correlation between changes in the intestinal microbiota and susceptibility to the development of airway allergies.

A reduction in the microbial variety in the intestine during childhood has been shown to increase the risk of developing asthma and the use of broad-spectrum antibiotics may increase the predisposition to allergic airway diseases thus demonstrating the correlation in the intestine-lung axis.

The respiratory tract, long considered sterile, is actually a dynamic, microbial ecosystem. Unlike the intestinal microbiota, the lower respiratory tract is one of the least populated sites by microorganisms in the human body, with an approximate number of 10— bacteria per 1, cells Its composition is dependent on microbial colonization of the upper respiratory tract through salivary micro-inhalations, interactions with the host's immune system and environmental conditions such as pH and oxygen concentration The intestine and lungs develop in parallel after birth, with constant communication between these two compartments with the bacterial phyla most common in the lower respiratory tract being the same as those in the intestine, mainly Firmicutes and Bacteroidetes, followed by Proteobacteria and Actinobacteria On the other hand, the nasal microbiota is more similar to skin microbiota, with a prevalence of Firmicutes and Actinobacteria phyla 48 , The mesenteric lymphatic system is an important communication route between the intestine and the lungs, through which intact bacteria, their fragments or metabolites can translocate through the intestinal barrier, reach the circulatory system, and modulate the lung's immune response For example SCFAs, which are mainly synthesized through the fermentation of bacterial dietary fibers, act in the lungs as signaling molecules in cells presenting resident antigens, thereby reducing inflammatory and allergic responses However, the gut-lung cross-talk also can influence in the opposite way, when the lung infections or chronic inflammatory diseases induce alterations in gut microbiota.

Chronic lung disorders, such as asthma and COPD, can exhibit not only dysbiosis in airway microbiota but also in gut microbiota with tissue damage In addition, respiratory influenza infections in mice indirectly induce intestinal immune injury and gut dysbiosis promoting inflammation through the outgrowth of Enterobacteriaceae and the reduction of Lactobacilli and Lactococci Still during mice influenza infection, changes in gut microbiota composition, reduce the acetate production and affect the bactericidal activity of alveolar macrophages contributing to pulmonary pneumococcal superinfection.

However, it has been shown that intranasal administration of Lactobacillus casei may be able to protect and mitigate the symptoms from influenza virus infection in neonatal and infant mice infected.

Intranasal Bifidobacterium longum administration also protects against viral-induced lung inflammation and injury in murine model of influenza virus infection In this study, the reduced viral load was associated with reduced lung injury and IL-6 inflammatory cytokine, besides a shift from neutrophil to macrophage recruitment and increased levels of IFN-λ and surfactant protein.

The intranasal administration probiotics has also been used in inflammatory lung diseases. A study with 24 patients with chronic rhinosinusitis showed benefits with of Lactococcus lactis W bacteria i ntranasal irrigation after 14 days, with increase of the Dolosigranulum pigrum , a bacteria identified as potentially beneficial in the upper airways Another study in a mouse model of allergic asthma reported that intranasal administration of probiotic Lactobacillus rhamnosus GG prevents the development of asthma due to decrease in bronchoalveolar lavage the eosinophils cells, lung IL-5 and 13 levels, and airway hyperreactivity This way, modifications in airway microbiota can contribute to protection against infections and inflammatory lung diseases.

Together, these data show the importance of gut-lung cross-talk in maintaining pulmonary mucosa homeostasis, as well as in the immune response against pathogens and the development of inflammatory diseases.

Epigenetics is the transcriptional regulation of gene expression carried out by chemical changes in DNA, such as methylation, acetylation, phosphorylation, and regulation by miRNAs microRNA , which result in phenotypic changes without promoting changes in the DNA sequence , Transcriptional changes by acetylation are mediated by histone deacetylases HDACs and histone acetyltransferases HATs.

The deacetylation of histone lysine residues mediated by HDACs makes chromatin transcriptionally repressive, interfering with gene expression by inhibiting the access of transcription factors , HAT-mediated histone acetylation makes chromatin transcriptionally permissive, thus favoring the binding of transcription factors and other transcriptional coactivators , In addition to histones, HDACs have other protein substrates, such as NF-κB.

Sirtuin I SIRT1 , a class III HDAC, in addition to acting on histones, also acts on NF-κB, promoting deacetylation of the p65 subunit. Therefore, SIRT1 acts to suppress the transcription of proinflammatory cytokines HDAC and HAT activity has already been identified in nuclear extracts from lung-tissue specimens.

Moreover, it has been reported that patients with COPD have a progressive reduction in total HDAC activity, reflecting the severity of the disease HDACs are key molecules in suppressing the production of proinflammatory cytokines; they are understood to be an important component that can act on lung health.

Bioactive compounds may play roles in the regulation of HDAC activity and histone acetylation Bioactive compounds are extranutritional constituents that are usually present in food in small concentrations and provide health benefits beyond basic nutritional value These bioactive molecules can have therapeutic potential by influencing energy intake, in addition to reducing the proinflammatory state, oxidative stress and metabolic disorders Epidemiological studies suggest that the increase in consumption of foods rich in bioactive compounds with antioxidant activity, such as vitamins, phytochemicals, and especially phenolic compounds, may represent an important factor in the reduction of several pathologies, such as cancer, heart disease, stroke, and Alzheimer's disease Resveratrol is a polyphenolic bioactive compound found in several plant species, including grapes and peanuts, and is able to positively regulate SIRT1 in human pulmonary alveolar epithelial cells, reduce the production of ROS and inhibit apoptosis in alveolar epithelial cells, thus reducing lung injury It has also been reported that SIRT1 activates peroxisome proliferator-activated receptor-gamma coactivator PGC -1α, an important regulator of mitochondrial metabolism.

Therefore, resveratrol can improve mitochondrial function, which is usually compromised in the lungs of patients with COPD In the context of viral infections, in vitro studies have indicated that treatment with a SIRT1 antagonist EX generates an increase in the production of influenza viruses and human cytomegalovirus HCMV infection, while SIRT1 agonists promote a reduction in the production of viral particles Studies have also indicated a potential role for SIRT1 in regulating inflammation during allergic asthma due to significant inhibition of IL-6 expression However, most of the proposed therapeutic activities of resveratrol have not yet been confirmed in clinical trials.

There are reports that in healthy individuals, a single dose of resveratrol mg combined with muscadine grape extract polyphenols 75 mg is able to suppress the oxidative and inflammatory response to stress However, more studies are needed.

Another bioactive compound, diferuloylmethane, is also capable of inducing epigenetic regulation and contributing to lung health. Known as curcumin or turmeric from India, this compound has a pleiotropic role, interacting with several molecular targets, such as transcription factors, proteins and enzymes associated with epigenetic modulations Therefore, it promotes the suppression of histone acetylation and simultaneously promotes active activation to HDAC2 deacetylation, canceling the interaction between NF-κB and DNA; thus, preventing inflammatory responses that may be harmful to lung tissue Considering that corticosteroids recruit HDAC2 as one of the mechanisms of action, it has been suggested that its induction through curcumin may be an important therapeutic target Curcumin also has direct anti-inflammatory actions through the inhibition of inhibition of IκB kinase IKK , which degrades κB, a molecule capable of degrading the inhibitory protein of the NF-κB complex In the context of viral infections, it has been reported that curcumin can provide protection against acute lung injuries induced by H1N1 infection by limiting the expansion of immune cells and reducing the production of proinflammatory cytokines via NF-κB The safe dose of curcumin is 12 grams per day; however, there are few clinical studies that have shown that ingesting curcumin can have anti-inflammatory effects, considering that one of its main disadvantages is its low bioavailability and hydrophobic nature Another compound that can influence lung health includes catechins.

Catechins are among the biologically active compounds present in Camellia sinensis , known as green tea, and they are tea's main antioxidant agent. The catechins contained in tea include epigallocatechingallate EGCG , epicatechingallate ECG , epigallocatechin EGC , and epicatechin EC Among these, EGCG is the catechin that most demonstrates therapeutic effects.

EGCG is shown to be a specific inhibitor of HAT, thus influencing histone acetylation and promoting an anti-inflammatory effect by inhibiting the Pmediated acetylation of NK-κB. Moreover, it is also able to prevent the binding of p Its anti-inflammatory effect is mediated by inhibition of pmediated acetylation with the NK-κB promoter It is described that ingestion through catechin feeding is able to improve lung health and to reduce shortness of breath and sputum in COPD However, further studies are needed to evaluate the most safe and effective dosage.

SARS-CoV-2 quickly spread around the world in , and has been classified as a global pandemic by the World Health Organization This virus is the etiologic agent of coronavirus disease COVID which presents, in general, mild, and moderate symptoms, but a more severe manifestation can cause acute respiratory syndrome, multiple organ dysfunction syndrome and can lead to death , Indeed, a little over a year and a half after the first case of the disease, more than Taking into account the anti-inflammatory and immunoprotective role that nutrients play in the pulmonary mucosa already discussed in the course of this review, it is not absurd to think that nutrients can be used as an important strategy against SARS-CoV-2 infection Figure 3.

Indeed, some studies, mostly using vitamins and antioxidant nutrients or demonstrating their deficiencies, have already shown some effect during COVID, as we describe below.

Figure 3. Possible role of nutrients in COVID pulmonary pathophysiology. Some nutrients have been proposed during COVID A Naringenin has been described as being able to inhibit infection SARS-CoV-2 infection.

B Vitamins, minerals, and flavonoids can inhibit viral replication in many pulmonary infections, and naringenin already demonstrated ability to decrease viral replication of SARS-CoV C These nutrients also have antioxidant role inhibition of reactive oxygen species—ROS and D anti-inflammatory activity inhibition of transcription proinflammatory factors transcription and may inhibit the deleterious effects of the cytokine storm and tissue damage present in COVID In addition, vitamin D demonstrated a relevant role on glucose-treated monocytes, lowering the risk of oxidative stress and the release of IL-8 and CCL-2 by monocytes.

This can be relevant since diabetes is considered a risk factor in COVID patients, in addition to the fact that monocytes glycolysis is a mechanism used by SARS-CoV-2 to promote inhibition of T cells and tissue damage in the lungs.

Perhaps the most prominent vitamin in this context is vitamin D. Many studies have already identified that there is a high incidence of vitamin D deficiency in patients with SARS-CoV-2 infection — In addition, these studies have also shown a relationship between the level of vitamin D deficiency and the severity of COVID There have been many hypotheses suggested for this relationship, since the anti-inflammatory capacity of vitamin D is very important in a pathology characterized by a proinflammatory cytokine storm that worsens the patient's clinical condition until the possibility of affecting the need for oxygen-support therapy in patients with COVID This deficiency is also related to the risk of mortality from the disease In an in vitro study with high glucose-treated monocytes, combined supplementation with vitamin D and l-cysteine was effective in lowering the risk of oxidative stress and the release of IL-8 and C—C motif chemokine ligand 2 CCL-2 by monocytes This can be relevant in patients with type 2 diabetes and COVID infection, since diabetes is considered a risk factor Moreover, it was recently demonstrated that monocytes play an important role in COVID pathogenicity, since SARS-CoV-2 infection triggers mitochondrial ROS production in monocytes and promotes glycolysis, inhibiting the T cell response and epithelial-cell survival in the lungs Thus, the ability of vitamin D to suppress glucose-treated monocytes can be very important during SARS-CoV-2 infection.

Vitamins A, C and E have also demonstrated some importance in the prognosis of patients with COVID, since their deficiencies have been reported, especially in the most severe COVID patients Possibly, the antiviral and anti-inflammatory activity exerted by these nutrients must be impaired in those patients whose vitamin deficiency is more pronounced.

In this way, vitamin supplementation in these patients is strongly suggested Another kind of nutrient deficiency in COVID patients is minerals with antioxidant activity, such as selenium, zinc, magnesium, and copper , which are essential in controlling the oxidative stress induced by SARS-CoV-2 infection.

Among flavonoids, naringenin has been shown to be a powerful inhibitor of SARS-CoV-2 infection in vitro decreasing viral replication in Vero E6 lineage cells, demonstrating an important role in the control of viral load. In this way, naringenin can be a possible component in the treatment of patients with SARS-CoV-2 infection.

All of these data show that nutrients, in general, play an important role in the control of SARS-CoV-2 infection, which can be used as treatment strategies that may reduce the length of hospital stays and the need for respiratory support in these patients.

However, more studies need to be carried out to better define the role that each nutrient may have in COVID prognosis, given the vast anti-inflammatory and antiviral action that each nutrient can exert on the lung environment and the immune system in general.

The nutrients addressed in this review, in addition to their nutritional role, have a relevant role in maintaining lung health; therefore, adequate consumption of these nutrients is essential to promote an efficient immune response in the control of inflammatory diseases and infections.

Moreover, the in vitro use of some nutrients with antiviral activity has been shown to be efficient against SARS-CoV-2 infections, which highlights the importance of these components in the current moment of the pandemic that we are facing.

SG-S and LO performed conception, and write and review. FT performed conception, write, and illustration and review. MS performed conception and review. AD performed review. All authors contributed to the article and approved the submitted version.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers.

Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher. Sahan E, Sahan S, Karamanlioglu M. These are fats that are often liquid at room temperature and come from plant sources, such as canola, safflower and corn oils.

Limit foods that contain trans fats and saturated fat. For example, butter, lard, fat and skin from meat, hydrogenated vegetable oils, shortening, fried foods, cookies, crackers and pastries. Many people find taking a general-purpose multivitamin helpful. Often, people with COPD take steroids.

Long-term use of steroids may increase your need for calcium. Consider taking calcium supplements. Look for one that includes vitamin D. Calcium carbonate or calcium citrate are good sources of calcium. Before adding any vitamins to your daily routine, be sure to discuss with your doctor.

Too much sodium may cause edema swelling that may increase blood pressure. If edema or high blood pressure are health problems for you, talk with your doctor about how much sodium you should be eating each day. Ask your RDN about the use of spices and herbs in seasoning your food and other ways you can decrease your sodium intake.

Drinking plenty of water is important not only to keep you hydrated, but also to help keep mucus thin for easier removal. Talk with your doctor about your water intake.

A good goal for many people is 6 to 8 glasses 8 fluid ounces each daily. Don't try to drink this much fluid at once; spread it out over the entire day. Some people find it helpful to fill a water pitcher every morning with all the water they are supposed to drink in one day.

They then refill their glass from that pitcher and keep track of their progress during the course of the day. Remember, any healthy caffeine-free fluid counts toward your fluid goal, and most foods contribute a substantial amount of fluid, as well.

You may find it difficult to meet your nutritional needs with regular foods, especially if you need a lot of calories every day. Also, if your RDN has suggested that you get more of your calories from fat—the polyunsaturated, monounsaturated, and low-cholesterol variety—you may not be able to meet this goal easily with ordinary foods.

Your RDN or doctor may suggest you drink a liquid called a medical nutritional product supplement. Some of these products can be used as a complete diet by people who can't eat ordinary foods, or they can be added to regular meals by people who can't eat enough food.

Read more on our Each Breath Blog about COPD and Nutrition: Managing Difficulties with Weight Gain. Get in the habit of weighing yourself regularly. The scale will alert you to weight loss or gain.

You should see your doctor or dietitian if you continue to lose weight or if you gain weight while following the recommended diet. There are health complications that can result from being underweight or overweight.

A well-nourished body is better able to handle infections. When people with COPD get an infection, it can become serious quickly and result in hospitalization. Good nutrition can help prevent that from happening.

If illness does occur, a well-nourished body can respond better to treatment. Note: These are general nutritional guidelines for people living with COPD. Each person's needs are different, so talk to your doctor or RDN before you make changes to your diet.

Reviewed and approved by the American Lung Association Scientific and Medical Editorial Review Panel. Join over , people who receive the latest news about lung health, including research, lung disease, air quality, quitting tobacco, inspiring stories and more!

Your tax-deductible donation funds lung disease and lung cancer research, new treatments, lung health education, and more.

They share their experiences…. A healthy and well-balanced diet and adequate nutrition are important in keeping as well as possible when living with a lung condition such as Chronic Obstructive Pulmonary Disease COPD or bronchiectasis.

Why is hydration important for our lung health? How much fluid should I drink? What fluids should I drink? What are the impacts of being underweight on lung function? What are the most important foods to eat if I struggle to eat too much?

Tips: Protein-rich foods include meat, fish, eggs, dairy products, beans, lentils, nuts and tofu. If your weight is stable, you should aim to eat protein-rich foods at least 3 times a day, but if you have a poor appetite or have been losing weight, you should aim to include protein-rich foods between meals as well.

Your GP or healthcare team may also recommend an oral nutrition supplement , which is a special drink made up of proteins, vitamins, minerals, calories as well as fluids.

Low vitamin D levels are associated with lower lung function and an increased risk of infection. Vitamin D is also essential for bone health, so try and get vitamin D from the sun by spending a few minutes outdoors on most days of the week. In winter, spend some time outdoors with some skin uncovered in the middle of the day.

If you find your vitamin D levels are low, a vitamin D supplement may be required. What foods are good for my lung health? Tips: Try to eat two serves of fruits, and five serves of vegetables a day Fibre can be found in fruits, vegetables, legumes, nuts, and wholegrain foods such as brown rice, oatmeal, and couscous.

There is some research suggesting a high fibre diet can help prevent reductions in lung function Omega-3 fatty acids can be found in salmon, sardines, mackerel, herring, or an omega-3 supplement Choose good quality fats such as extra virgin olive oil, nuts and nut butters, seeds, and avocado.

What foods should I avoid? January 10 Exercising with a lung condition in hot weather. Read More. In particular, we welcome exploration of the interplay between diet and the gut-lung axis, and how these interactions modulate respiratory health.

We welcome proposals ranging from original research to review articles to contribute to a deeper understanding of these critical connections. Keywords : lung health, respiratory health, gut-lung axis, asthma, COVID, lung cancer, COPD, bronchitis, lungs, lung, breathing, gut health, respiratory disease.

Important Note : All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

No records found. total views article views downloads topic views. With their unique mixes of varied contributions from Original Research to Review Articles, Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area!

Find out more on how to host your own Frontiers Research Topic or contribute to one as an author. Overview Articles Authors Impact. About this Research Topic Manuscript Submission Deadline 06 March Keywords : lung health, respiratory health, gut-lung axis, asthma, COVID, lung cancer, COPD, bronchitis, lungs, lung, breathing, gut health, respiratory disease Important Note : All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements.

Sort by: Views Type Date Views Views Type Date.