Adipose tissue as a potential source of hormones and cytokines involved in asthma pathogenesis

Abstract

Asthma and obesity are chronic inflammatory diseases affecting millions of people worldwide. Numerous epidemiological data have revealed increased adiposity as a potential risk factor for severity and incidence of asthma. In addition, obesity is not only risk factor for asthma but is also related to its poor control. Despite the mechanism underlying obesity–asthma relation is not fully understood, it has been proposed that the common inflammatory mechanism plays a crucial role in determination of this relation. Adipose tissue is referred as extremely active endocrine organ secreting numerous hormones and cytokines that regulate immune responses and metabolism. In the lean state, the high levels of anti-inflammatory adipokines such as adiponetctin as well as low levels of pro-inflammatory adipokines i.e. leptin, and pro-inflammatory cytokines such as TNF-α, IL-8, IL-6 are secreted by adipose tissue. On the other hand, in the obese state, hypertrophic adipocytes and activated macrophages produce decreased level of adiponectin and increased levels of pro-inflammatory adipokines and cytokines leading to “metabolic inflammation”. It may be possible that these obesity-related pro-inflammatory adipokines may be associated with airway inflammation in obesity-related asthma. In the current review, we summarized the recent knowledge concerning possible molecular mechanisms mediating the relation between obesity and asthma.