Abstract
Background. The prevalence of obesity has increased dramatically over the last decades, and its association with asthma is being increasingly recognized. Aims. Our hypothesis is that increased leptin and decreased adiponectin levels in obese subjects play a direct role in regulating inflammation in asthmatics. We wanted to examine the hypothesis that cysteinyl leukotrienes (cys-LT), inflammatory mediators that are regulated by adipokines, are involved in the pathogenesis of asthma. Methods. We studied a population of asthmatics and nonasthmatics, who in turn were divided into obese and nonobese categories. We examined leptin and its ratio to adiponectin, in asthmatics and nonasthmatics, with and without obesity. In addition, we measured cys-LT levels in exhaled breath condensate (EBC) and in peripheral blood monocytes (PBM) in these groups. Results. Leptin levels were increased in obese asthmatics compared to obese nonasthmatics. The leptin/adiponectin (L/A) ratio was higher in obese asthmatics compared to obese nonasthmatics. EBC cys-LT levels were elevated in asthmatics compared to nonasthmatics. Discussion. Proinflammatory adipokines, released from adipose tissue, may promote an asthma phenotype through enhanced cys-LT production that may result in more prevalent and difficult to control airway disease.
Highlights
Over the past 30 years there has been a dramatic increase in the prevalence in obesity in the US, from 18% in the 80s to approximately 35% in 2010 [1, 2]
In view of the positive association between leptin and LT level, we examined cys-LT levels in the exhaled breath condensate (EBC) and peripheral blood leukocytes of asthmatics compared to nonasthmatics and obese compared to nonobese subjects
The main findings of this study are the following: (1) plasma leptin levels are increased in obese asthmatics compared to obese nonasthmatics
Summary
Over the past 30 years there has been a dramatic increase in the prevalence in obesity in the US, from 18% in the 80s to approximately 35% in 2010 [1, 2]. Obesity is independently associated with increased bronchial hyperresponsiveness [6]. The prevalence of obesity has increased dramatically over the last decades, and its association with asthma is being increasingly recognized. Our hypothesis is that increased leptin and decreased adiponectin levels in obese subjects play a direct role in regulating inflammation in asthmatics. We examined leptin and its ratio to adiponectin, in asthmatics and nonasthmatics, with and without obesity. Leptin levels were increased in obese asthmatics compared to obese nonasthmatics. The leptin/adiponectin (L/A) ratio was higher in obese asthmatics compared to obese nonasthmatics. EBC cys-LT levels were elevated in asthmatics compared to nonasthmatics. Proinflammatory adipokines, released from adipose tissue, may promote an asthma phenotype through enhanced cys-LT production that may result in more prevalent and difficult to control airway disease
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