Features of cytokine and adipokine regulation in asthma associated with obesity

摘要

The aim is to establish interrelations between levels of cytokines and adipokines in blood serum of patients with asthma; to reveal the features of cytokine and adipokine regulation in asthma associated with obesity. Material and Methods ― We examined 71 patients with partially controlled mild asthma: 24 normal-weight patients (group 1), 24 overweight patients (group 2), 23 patients with grade I and II obesity (group 3). The control group consisted of 25 healthy volunteers. Blood serum levels of Tumour necrosis factor alpha (TNF-α), interferon gamma (IFN-γ), interleukin-2 (IL-2), IL-4, IL-6, IL-10, and IL-17A were studied by flow cytometry. The concentrations of leptin and adiponectin were measured by an enzyme immunoassay. Results ― Increase levels of TNF-α, IL-6, IL-17A and IL-4 have been found in asthma patients regardless of body weight. At the same time, IL-6 level in the groups 2 and 3 was 1.4 times higher than in group 1. IL-17A level in patients with asthma and obesity was 1.2 times higher than in the groups 1 and 2. The elevation of IL-10 level in 1.8 and 2.3 times in patients of groups 2 аnd 3 in comparison with the group 1, respectively, has been determined. Hyperleptinemia was detected in the groups 2 and 3. A positive correlation between the body mass index and the levels of leptin, IL-4, IL-6, IL-10, IFN-γ and an invert correlation between this index and adiponectin concentration has been established. The interrelations between the levels of leptin, pro- and anti-inflammatory cytokines, depending on the body weight, have been revealed. Conclusion ― The production of pro-inflammatory cytokines IL-6 and IL-17A, as well as anti-inflammatory cytokine IL-10 enhances in asthma patients as the body weight increases and the obesity develops. The features of cytokine and adipokine imbalance indicate the prevalence of neutrophilic inflammation in asthma with obesity and demonstrates pathogenetic link between obesity and asthma.