A high-fat challenge increases airway inflammation and impairs bronchodilator recovery in asthma

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 fatconsumed. Ahigh-fat meal also suppresses bronchodilator recovery in asthma. Modifying dietary fat intake may beuseful in asthma.