Lisa G Wood1, Manohar L Garg, Peter G Gibson. 1. Centre for Asthma and Respiratory Disease, Hunter Medical Research Institute, University of Newcastle, Newcastle, Australia. lisa.wood@newcastle.edu.au
Abstract
BACKGROUND:Dietary fat activatessystemic 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 plasmaTNF-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 4mRNA 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. 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.
RCT Entities:
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 obesepatients 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 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. 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.
Authors: Cynthia W Baffi; Lisa Wood; Daniel Winnica; Patrick J Strollo; Mark T Gladwin; Loretta G Que; Fernando Holguin Journal: Chest Date: 2016-01-20 Impact factor: 9.410