title: The influence of obesity on inflammation and clinical symptoms in asthma.
abstract: Obesity and asthma are both important public health issues. Increasing number of studies suggest the association between obesity and asthma which may be causal or accidental. The studies on animal models show innate enhancement of airway hyper-responsiveness which suggest that chronic airway hyper-responsiveness may be related to chronic low-grade systemic inflammation occurring in obesity. These results are confirmed by studies on asthmatic patients which show that levels of inflammation markers were higher in obese asthma patients and are related to the parameters of obesity. However, adipokines secreted by adipose tissue have also been involved in the regulation of inflammation and allergic responses, and suggested to affect the risk of asthma, especially in obese female patients. The studies on the association between adiposity and atopy have conflicting results and the issue needs to be investigated in the future. Obesity also decreases lung volume and increases airway resistance inducing symptoms that could mimic asthma. Clinical studies suggest that asthma in obese subjects may differ from the classical phenotype of the disease. Obese patients referred for asthma exacerbation present a reduced response to standard asthma medications. The review indicates that mechanical and inflammatory effects of obesity may explain the influence on asthma. Further studies on the association between adiposity and atopy on airway inflammation may confirm the active role of fat tissue, not only simple mechanical impairment of the thorax movement. Longitudinal studies are needed to understand the association between asthma, and obesity, which may open new therapeutic options for asthma treatment in obese patients.
authors.affiliation: Department of Allergology, Medical University of Gdansk, Gdansk, Poland. mg@gumed.edu.pl
authors.forename: M
authors.initials: M
authors.lastname: Gruchała-Niedoszytko
authors.forename: S
authors.initials: S
authors.lastname: Małgorzewicz
authors.forename: M
authors.initials: M
authors.lastname: Niedoszytko
authors.forename: M
authors.initials: M
authors.lastname: Gnacińska
authors.forename: E
authors.initials: E
authors.lastname: Jassem
mesh_terms: D054392:Adipokines / Q000378:metabolism; D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D001249:Asthma / Q000150:complications* / Q000503:physiopathology; D016535:Bronchial Hyperreactivity / Q000503:physiopathology; D004195:Disease Models, Animal; D005260:Female; D006801:Humans; D007249:Inflammation / Q000150:complications* / Q000503:physiopathology; D008297:Male; D009765:Obesity / Q000150:complications* / Q000503:physiopathology; D010641:Phenotype; D012129:Respiratory Function Tests; D012307:Risk Factors
chemical_list: D054392:Adipokines