A high-fat challenge increases airway inflammation and impairs bronchodilator recovery in asthma - 11/08/11
Abstract |
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-⍺, 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.
El texto completo de este artículo está disponible en PDF.Key words : Dietary fat, fatty acids, neutrophils, Toll-like receptor 4, innate immunity, asthma, bronchodilator recovery, airway inflammation
Abbreviations used : ACQ, AHF, AHF-NonO, AHF-O, ALF, BMI, CRP, DRS, eNO, FVC, HCHF, MUFA, NF-κB, PUFA, SFA, TE, TLR
Esquema
Supported by a National Health and Medical Research Council of Australia Project Grant and a Hunter Medical Research Institute project grant sponsored by the Piggott family. |
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Disclosure of potential conflict of interest: L. G. Wood has received honoraria from GlaxoSmithKline and has received research support from the National Health and Medical Research Council. M. L. Garg declares no conflicts of interest. P. G. Gibson has received honoraria from GlaxoSmithKline and Boehringer Ingelheim and has received research support from the National Health and Medical Research Council. |
Vol 127 - N° 5
P. 1133-1140 - mai 2011 Regresar al númeroBienvenido a EM-consulte, la referencia de los profesionales de la salud.
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