A high-fat challenge increases airway inflammation and impairs bronchodilator recovery in asthma
Dietary fat activates systemic innate immune responses, but the effect on airway responses is unknown. To examine effects of a high-fat versus low-fat meal on systemic and airway inflammation in asthma. Nonobese subjects with asthma were randomized to consume a high-fat (n = 19; 48% [49 g] fat) or l...
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| Published in | Journal of allergy and clinical immunology Vol. 127; no. 5; pp. 1133 - 1140 |
|---|---|
| Main Authors | , , |
| Format | Journal Article |
| Language | English |
| Published |
New York, NY
Mosby, Inc
01.05.2011
Elsevier Elsevier Limited |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0091-6749 1097-6825 1097-6825 |
| DOI | 10.1016/j.jaci.2011.01.036 |
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| Abstract | Dietary fat activates systemic innate immune responses, but the effect on airway responses is unknown.
To examine effects of a high-fat versus low-fat meal on systemic and airway inflammation in asthma.
Nonobese subjects with asthma were randomized to consume a high-fat (n = 19; 48% [49 g] fat) or low-fat (n = 18; 15% [3 g] fat) meal. Fourteen obese patients with asthma and 21 healthy controls also consumed a high-fat meal. Another group of patients with asthma consumed a high-trans (n = 5; 5.2 g trans fat) or nontrans (n = 5, <0.3 g trans fat) fatty acid meal. Lung function was measured at baseline (prebronchodilator) and 2, 3, and 4 hours after bronchodilator. Airway inflammation was assessed by using induced sputum cell counts and Toll-like receptor 4 mRNA expression by real-time PCR. Systemic inflammation was measured by ELISA quantification of plasma TNF-α, high-sensitivity C-reactive protein, and IL-6 concentrations.
In patients with asthma, at 4 hours postmeal, increases in sputum % neutrophils and Toll-like receptor 4 mRNA expression were higher and increases in FEV
1/forced vital capacity (FVC) were lower in the high-fat versus low-fat groups. Changes in plasma fatty acids correlated with changes in sputum % neutrophils and were negatively associated with changes in % FEV
1, % FVC, and FEV
1/FVC. After the high-trans fatty acid meal, sputum % neutrophils were significantly higher than after the nontrans meal.
A high-fat meal augments neutrophilic airway inflammation, with the effect dependent on the type of fat consumed. A high-fat meal also suppresses bronchodilator recovery in asthma. Modifying dietary fat intake may be useful in asthma. |
|---|---|
| AbstractList | BACKGROUND: Dietary fat activates systemic innate immune responses, but the effect on airway responses is unknown. OBJECTIVE: To examine effects of a high-fat versus low-fat meal on systemic and airway inflammation in asthma. METHODS: Nonobese subjects with asthma were randomized to consume a high-fat (n = 19; 48% [49 g] fat) or low-fat (n = 18; 15% [3 g] fat) meal. Fourteen obese patients with asthma and 21 healthy controls also consumed a high-fat meal. Another group of patients with asthma consumed a high-trans (n = 5; 5.2 g trans fat) or nontrans (n = 5, <0.3 g trans fat) fatty acid meal. Lung function was measured at baseline (prebronchodilator) and 2, 3, and 4 hours after bronchodilator. Airway inflammation was assessed by using induced sputum cell counts and Toll-like receptor 4 mRNA expression by real-time PCR. Systemic inflammation was measured by ELISA quantification of plasma TNF-α, high-sensitivity C-reactive protein, and IL-6 concentrations. RESULTS: In patients with asthma, at 4 hours postmeal, increases in sputum % neutrophils and Toll-like receptor 4 mRNA expression were higher and increases in FEV₁/forced vital capacity (FVC) were lower in the high-fat versus low-fat groups. Changes in plasma fatty acids correlated with changes in sputum % neutrophils and were negatively associated with changes in % FEV₁, % FVC, and FEV₁/FVC. After the high-trans fatty acid meal, sputum % neutrophils were significantly higher than after the nontrans meal. CONCLUSION: A high-fat meal augments neutrophilic airway inflammation, with the effect dependent on the type of fat consumed. A high-fat meal also suppresses bronchodilator recovery in asthma. Modifying dietary fat intake may be useful in asthma. Background Dietary fat activates systemic innate immune responses, but the effect on airway responses is unknown. Objective To examine effects of a high-fat versus low-fat meal on systemic and airway inflammation in asthma. Methods Nonobese subjects with asthma were randomized to consume a high-fat (n = 19; 48% [49 g] fat) or low-fat (n = 18; 15% [3 g] fat) meal. Fourteen obese patients with asthma and 21 healthy controls also consumed a high-fat meal. Another group of patients with asthma consumed a high-trans (n = 5; 5.2 g trans fat) or nontrans (n = 5, <0.3 g trans fat) fatty acid meal. Lung function was measured at baseline (prebronchodilator) and 2, 3, and 4 hours after bronchodilator. Airway inflammation was assessed by using induced sputum cell counts and Toll-like receptor 4 mRNA expression by real-time PCR. Systemic inflammation was measured by ELISA quantification of plasma TNF-α, high-sensitivity C-reactive protein, and IL-6 concentrations. Results In patients with asthma, at 4 hours postmeal, increases in sputum % neutrophils and Toll-like receptor 4 mRNA expression were higher and increases in FEV1/forced vital capacity (FVC) were lower in the high-fat versus low-fat groups. Changes in plasma fatty acids correlated with changes in sputum % neutrophils and were negatively associated with changes in % FEV1, % FVC, and FEV1/FVC. After the high-trans fatty acid meal, sputum % neutrophils were significantly higher than after the nontrans meal. Conclusion A high-fat meal augments neutrophilic airway inflammation, with the effect dependent on the type of fat consumed. A high-fat meal also suppresses bronchodilator recovery in asthma. Modifying dietary fat intake may be useful in asthma. Dietary fat activates systemic innate immune responses, but the effect on airway responses is unknown.BACKGROUNDDietary fat activates systemic innate immune responses, but the effect on airway responses is unknown.To examine effects of a high-fat versus low-fat meal on systemic and airway inflammation in asthma.OBJECTIVETo examine effects of a high-fat versus low-fat meal on systemic and airway inflammation in asthma.Nonobese subjects with asthma were randomized to consume a high-fat (n = 19; 48% [49 g] fat) or low-fat (n = 18; 15% [3 g] fat) meal. Fourteen obese patients with asthma and 21 healthy controls also consumed a high-fat meal. Another group of patients with asthma consumed a high-trans (n = 5; 5.2 g trans fat) or nontrans (n = 5, <0.3 g trans fat) fatty acid meal. Lung function was measured at baseline (prebronchodilator) and 2, 3, and 4 hours after bronchodilator. Airway inflammation was assessed by using induced sputum cell counts and Toll-like receptor 4 mRNA expression by real-time PCR. Systemic inflammation was measured by ELISA quantification of plasma TNF-α, high-sensitivity C-reactive protein, and IL-6 concentrations.METHODSNonobese subjects with asthma were randomized to consume a high-fat (n = 19; 48% [49 g] fat) or low-fat (n = 18; 15% [3 g] fat) meal. Fourteen obese patients with asthma and 21 healthy controls also consumed a high-fat meal. Another group of patients with asthma consumed a high-trans (n = 5; 5.2 g trans fat) or nontrans (n = 5, <0.3 g trans fat) fatty acid meal. Lung function was measured at baseline (prebronchodilator) and 2, 3, and 4 hours after bronchodilator. Airway inflammation was assessed by using induced sputum cell counts and Toll-like receptor 4 mRNA expression by real-time PCR. Systemic inflammation was measured by ELISA quantification of plasma TNF-α, high-sensitivity C-reactive protein, and IL-6 concentrations.In patients with asthma, at 4 hours postmeal, increases in sputum % neutrophils and Toll-like receptor 4 mRNA expression were higher and increases in FEV(1)/forced vital capacity (FVC) were lower in the high-fat versus low-fat groups. Changes in plasma fatty acids correlated with changes in sputum % neutrophils and were negatively associated with changes in % FEV(1), % FVC, and FEV(1)/FVC. After the high-trans fatty acid meal, sputum % neutrophils were significantly higher than after the nontrans meal.RESULTSIn patients with asthma, at 4 hours postmeal, increases in sputum % neutrophils and Toll-like receptor 4 mRNA expression were higher and increases in FEV(1)/forced vital capacity (FVC) were lower in the high-fat versus low-fat groups. Changes in plasma fatty acids correlated with changes in sputum % neutrophils and were negatively associated with changes in % FEV(1), % FVC, and FEV(1)/FVC. After the high-trans fatty acid meal, sputum % neutrophils were significantly higher than after the nontrans meal.A high-fat meal augments neutrophilic airway inflammation, with the effect dependent on the type of fat consumed. A high-fat meal also suppresses bronchodilator recovery in asthma. Modifying dietary fat intake may be useful in asthma.CONCLUSIONA high-fat meal augments neutrophilic airway inflammation, with the effect dependent on the type of fat consumed. A high-fat meal also suppresses bronchodilator recovery in asthma. Modifying dietary fat intake may be useful in asthma. Dietary fat activates systemic innate immune responses, but the effect on airway responses is unknown. To examine effects of a high-fat versus low-fat meal on systemic and airway inflammation in asthma. Nonobese subjects with asthma were randomized to consume a high-fat (n = 19; 48% [49 g] fat) or low-fat (n = 18; 15% [3 g] fat) meal. Fourteen obese patients with asthma and 21 healthy controls also consumed a high-fat meal. Another group of patients with asthma consumed a high-trans (n = 5; 5.2 g trans fat) or nontrans (n = 5, <0.3 g trans fat) fatty acid meal. Lung function was measured at baseline (prebronchodilator) and 2, 3, and 4 hours after bronchodilator. Airway inflammation was assessed by using induced sputum cell counts and Toll-like receptor 4 mRNA expression by real-time PCR. Systemic inflammation was measured by ELISA quantification of plasma TNF-α, high-sensitivity C-reactive protein, and IL-6 concentrations. In patients with asthma, at 4 hours postmeal, increases in sputum % neutrophils and Toll-like receptor 4 mRNA expression were higher and increases in FEV(1)/forced vital capacity (FVC) were lower in the high-fat versus low-fat groups. Changes in plasma fatty acids correlated with changes in sputum % neutrophils and were negatively associated with changes in % FEV(1), % FVC, and FEV(1)/FVC. After the high-trans fatty acid meal, sputum % neutrophils were significantly higher than after the nontrans meal. A high-fat meal augments neutrophilic airway inflammation, with the effect dependent on the type of fat consumed. A high-fat meal also suppresses bronchodilator recovery in asthma. Modifying dietary fat intake may be useful in asthma. Dietary fat activates systemic innate immune responses, but the effect on airway responses is unknown. To examine effects of a high-fat versus low-fat meal on systemic and airway inflammation in asthma. Nonobese subjects with asthma were randomized to consume a high-fat (n = 19; 48% [49 g] fat) or low-fat (n = 18; 15% [3 g] fat) meal. Fourteen obese patients with asthma and 21 healthy controls also consumed a high-fat meal. Another group of patients with asthma consumed a high-trans (n = 5; 5.2 g trans fat) or nontrans (n = 5, <0.3 g trans fat) fatty acid meal. Lung function was measured at baseline (prebronchodilator) and 2, 3, and 4 hours after bronchodilator. Airway inflammation was assessed by using induced sputum cell counts and Toll-like receptor 4 mRNA expression by real-time PCR. Systemic inflammation was measured by ELISA quantification of plasma TNF-α, high-sensitivity C-reactive protein, and IL-6 concentrations. In patients with asthma, at 4 hours postmeal, increases in sputum % neutrophils and Toll-like receptor 4 mRNA expression were higher and increases in FEV 1/forced vital capacity (FVC) were lower in the high-fat versus low-fat groups. Changes in plasma fatty acids correlated with changes in sputum % neutrophils and were negatively associated with changes in % FEV 1, % FVC, and FEV 1/FVC. After the high-trans fatty acid meal, sputum % neutrophils were significantly higher than after the nontrans meal. A high-fat meal augments neutrophilic airway inflammation, with the effect dependent on the type of fat consumed. A high-fat meal also suppresses bronchodilator recovery in asthma. Modifying dietary fat intake may be useful in asthma. Background: Dietary fat activates systemic innate immune responses, but the effect on airway responses is unknown. Objective: To examine effects of a high-fat versus low-fat meal on systemic and airway inflammation in asthma. Methods: Nonobese subjects with asthma were randomized to consume a high-fat (n = 19; 48% [49 g] fat) or low-fat (n = 18; 15% [3 g] fat) meal. Fourteen obese patients with asthma and 21 healthy controls also consumed a high-fat meal. Another group of patients with asthma consumed a high-trans (n = 5; 5.2 g trans fat) or nontrans (n = 5, <0.3 g trans fat) fatty acid meal. Lung function was measured at baseline (prebronchodilator) and 2, 3, and 4 hours after bronchodilator. Airway inflammation was assessed by using induced sputum cell counts and Toll-like receptor 4 mRNA expression by real-time PCR. Systemic inflammation was measured by ELISA quantification of plasma TNF- alpha , high-sensitivity C-reactive protein, and IL-6 concentrations. Results: In patients with asthma, at 4 hours postmeal, increases in sputum % neutrophils and Toll-like receptor 4 mRNA expression were higher and increases in FEV sub(1/forced vital capacity (FVC) were lower in the high-fat versus low-fat groups. Changes in plasma fatty acids correlated with changes in sputum % neutrophils and were negatively associated with changes in % FEV) sub(1), % FVC, and FEV sub(1/FVC. After the high-trans fatty acid meal, sputum % neutrophils were significantly higher than after the nontrans meal. Conclusion: A high-fat meal augments neutrophilic airway inflammation, with the effect dependent on the type of fat consumed. A high-fat meal also suppresses bronchodilator recovery in asthma. Modifying dietary fat intake may be useful in asthma.) Background Dietary fat activates systemic innate immune responses, but the effect on airway responses is unknown. Objective To examine effects of a high-fat versus low-fat meal on systemic and airway inflammation in asthma. Methods Nonobese subjects with asthma were randomized to consume a high-fat (n = 19; 48% [49 g] fat) or low-fat (n = 18; 15% [3 g] fat) meal. Fourteen obese patients with asthma and 21 healthy controls also consumed a high-fat meal. Another group of patients with asthma consumed a high-trans (n = 5; 5.2 g trans fat) or nontrans (n = 5, <0.3 g trans fat) fatty acid meal. Lung function was measured at baseline (prebronchodilator) and 2, 3, and 4 hours after bronchodilator. Airway inflammation was assessed by using induced sputum cell counts and Toll-like receptor 4 mRNA expression by real-time PCR. Systemic inflammation was measured by ELISA quantification of plasma TNF-α, high-sensitivity C-reactive protein, and IL-6 concentrations. Results In patients with asthma, at 4 hours postmeal, increases in sputum % neutrophils and Toll-like receptor 4 mRNA expression were higher and increases in FEV1 /forced vital capacity (FVC) were lower in the high-fat versus low-fat groups. Changes in plasma fatty acids correlated with changes in sputum % neutrophils and were negatively associated with changes in % FEV1 , % FVC, and FEV1 /FVC. After the high-trans fatty acid meal, sputum % neutrophils were significantly higher than after the nontrans meal. Conclusion A high-fat meal augments neutrophilic airway inflammation, with the effect dependent on the type of fat consumed. A high-fat meal also suppresses bronchodilator recovery in asthma. Modifying dietary fat intake may be useful in asthma. |
| Author | Wood, Lisa G. Gibson, Peter G. Garg, Manohar L. |
| Author_xml | – sequence: 1 givenname: Lisa G. surname: Wood fullname: Wood, Lisa G. email: lisa.wood@newcastle.edu.au organization: Centre for Asthma and Respiratory Disease, Hunter Medical Research Institute, University of Newcastle, Newcastle, Australia – sequence: 2 givenname: Manohar L. surname: Garg fullname: Garg, Manohar L. organization: Nutraceuticals Research Group, School of Biomedical Sciences and Pharmacy, University of Newcastle, Newcastle, Australia – sequence: 3 givenname: Peter G. surname: Gibson fullname: Gibson, Peter G. organization: Centre for Asthma and Respiratory Disease, Hunter Medical Research Institute, University of Newcastle, Newcastle, Australia |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24163299$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/21377715$$D View this record in MEDLINE/PubMed |
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| Keywords | airway inflammation CRP DRS MUFA SFA NF-κB innate immunity HCHF TLR neutrophils BMI fatty acids PUFA Toll-like receptor 4 eNO Dietary fat asthma ACQ AHF-NonO TE FVC AHF-O ALF bronchodilator recovery AHF Total energy C-reactive protein Forced vital capacity Monounsaturated fatty acid Asthma low-fat/low-energy Body mass index Asthma high-fat/high energy—nonobese Toll-like receptor Healthy controls high-fat Exhaled nitric oxide Polyunsaturated fatty acid Asthma high-fat Nuclear factor-κB Asthma Control Questionnaire Dose response slope Saturated fatty acid Asthma high-fat/high energy—obese Toll like receptor 4 Granulocyte Lipids Natural immunity Respiratory system Recovery Respiratory tract Immunology Bronchus disease Obstructive pulmonary disease Lung disease Immunopathology Nutrition Respiratory disease Bronchodilator Increase Inflammation Fatty acids Feeding Asthma Diet Fat Neutrophil |
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| Snippet | Dietary fat activates systemic innate immune responses, but the effect on airway responses is unknown.
To examine effects of a high-fat versus low-fat meal on... Background Dietary fat activates systemic innate immune responses, but the effect on airway responses is unknown. Objective To examine effects of a high-fat... BACKGROUND: Dietary fat activates systemic innate immune responses, but the effect on airway responses is unknown. OBJECTIVE: To examine effects of a high-fat... Dietary fat activates systemic innate immune responses, but the effect on airway responses is unknown.BACKGROUNDDietary fat activates systemic innate immune... Background: Dietary fat activates systemic innate immune responses, but the effect on airway responses is unknown. Objective: To examine effects of a high-fat... |
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| SubjectTerms | Adult airway inflammation Allergy and Immunology Asthma Asthma - immunology Asthma - physiopathology Biological and medical sciences Bronchi - drug effects Bronchi - immunology Bronchi - physiopathology Bronchodilator Agents - pharmacology bronchodilator recovery bronchodilators C-reactive protein Chronic obstructive pulmonary disease, asthma Dietary fat Dietary Fats - administration & dosage Dietary Fats - immunology Dietary Fats - pharmacology enzyme-linked immunosorbent assay fat intake Fatty acids Fatty Acids - blood Female Fundamental and applied biological sciences. Psychology Fundamental immunology gene expression Humans Immune system Immunity, Innate - drug effects Immunopathology inflammation Inflammation - immunology innate immunity interleukin-6 lung function Male Medical sciences messenger RNA Middle Aged neutrophils Neutrophils - immunology Obesity - complications Obesity - immunology Oils & fats patients Pneumology quantitative polymerase chain reaction Respiratory System - drug effects Respiratory System - immunology Respiratory System - physiopathology Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis Sputum - immunology Toll-like receptor 4 Trans fats trans fatty acids Treatment Outcome tumor necrosis factor-alpha |
| Title | A high-fat challenge increases airway inflammation and impairs bronchodilator recovery in asthma |
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