Abstract
Consumption of a high fat meal can increase neutrophilic airway inflammation in asthma subjects. This study investigates the molecular mechanisms driving airway neutrophilia following a high fat meal in asthmatics. Subjects with asthma (n = 11) and healthy controls (n = 8) consumed a high-fat/energy meal, containing total energy (TE) of 3846 kJ and 48 g of total fat (20.5 g saturated). Sputum was induced at 0 and 4 h, and gene expression was examined by microarray and quantitative real-time PCR (qPCR). Following the high fat dietary challenge, 168 entities were significantly differentially expressed greater than >1.5 fold in subjects with asthma, whereas, in healthy controls, only 14 entities were differentially expressed. Of the 168 genes that were changed in asthma, several biological processes were overrepresented, with 25 genes involved in “immune system processes”. qPCR confirmed that S100P, S100A16, MAL and MUC1 were significantly increased in the asthma group post-meal. We also observed a strong correlation and a moderate correlation between the change in NLRP12 and S100A16 gene expression at 4 h compared to baseline, and the change in total and saturated non-esterified plasma fatty acid levels at 2 h compared to baseline. In summary, our data identifies differences in inflammatory gene expression that may contribute to increased airway neutrophilia following a high fat meal in subjects with asthma and may provide useful therapeutic targets for immunomodulation. This may be particularly relevant to obese asthmatics, who are habitually consuming diets with a high fat content.
Highlights
Asthma is a significant global disease which is a common source of morbidity and a significant cause of preventable mortality especially in Western countries, such as USA, Great Britain, Canada, Australia and New Zealand [1]
To investigate the effects of the high fat meal on airway inflammation, sputum gene expression was examined by microarray and confirmed using quantitative real-time PCR in a subset of subjects, and qPCR was subsequently performed on all asthmatic samples (n = 11)
We have previously demonstrated that a high fat intake increases neutrophilic airway inflammation in subjects with asthma [13]; we have a limited understanding of the inflammation in subjects with asthma [13]; we have a limited understanding of the molecular molecular mechanisms driving this effect
Summary
Asthma is a significant global disease which is a common source of morbidity and a significant cause of preventable mortality especially in Western countries, such as USA, Great Britain, Canada, Australia and New Zealand [1]. While allergen-induced T-helper type 2 immune activation leads to airway eosinophilia, asthma can involve innate immune dysfunction, with increased airway neutrophilia, sputum IL-8 and gene expression of TLR2 and TLR4 [2]. Stimuli that increase airway neutrophilia may contribute to asthma pathophysiology. As asthma prevalence has increased in recent decades and has been shown to develop in susceptible individuals who have migrated from a developing to a Westernized country [5,6,7], non-genetic, environmental factors, such as dietary intake, appear likely to be contributing to asthma
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