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.