Background: Obesity has become a lot more prevalent recently, and its involvement with pathogenesis of asthma is frequently investigated.
Aims: We hypothesize that altered plasma adipoikines and exhaled nitric oxide (NO) levels in obese subjects upregulate inflammation in asthmatics. We examined the hypothesis that the inflammatory mediators, cysteinyl leukotrienes (cys-LT) which are regulated by leptin and NO, play a role in the pathogenesis of airway inflammation in obese asthmatics.
Methods: We studied asthmatics (n=59) and non-asthmatics (n=58), both obese and non-obese, and further analyzed by gender. We examined plasma leptin, and fractional exhaled nitric oxide (FeNO), in obese and non-obese asthmatics and non-asthmatics. In addition, we measured urinary cys-LT levels in these subjects.
Results: Plasma leptin was increased in asthmatics compared to non-asthmatics (34.5±31 vs. 27.0±26, p=0.038), specifically in obese female asthmatics compared to obese male asthmatics (65.1±22.5 vs. 26.2±15.9 ng/ml, p=0.01). FeNO were decreased in obese compared to non-obese asthmatics (17.8±9.3 vs. 29.5±22.4, p=0.04), an effect that was most noted in female asthmatics. Urinary cys-LT levels were elevated in female asthmatic (7.2±2.9 vs. 5.0±1.8, p=0.002), especially in older heavier subjects. The ratio of urinary cys-LT to FeNO was elevated in obese female asthmatics.
Conclusions: Pro-inflammatory leptin and anti-inflammatory NO are altered in obese asthmatics. These mediators may regulate cys-LT. The group of subjects with elevated cys-LT/FeNO ratios may be a target for selective therapy.
Keywords: Obesity, leptin, nitric oxide, eicosanoid, airway