Regulation of lung inflammation by adiponectin

Abstract

Adiponectin is an insulin sensitizing hormone that also plays a role in the regulation of inflammation. Although adiponectin can exert pro-inflammatory effects, more studies have reported anti-inflammatory effects, even in non-adipose tissues such as the lung. Obesity is considered an inflammatory disease, is a risk factor for lung diseases, and is associated with decreased levels of plasma adiponectin. The results of recent studies have suggested that adiponectin exerts anti-inflammatory activity in chronic obstructive pulmonary disease, asthma and invasive fungal infection. The signaling receptors of adiponectin, AdipoR1 and AdipoR2, are expressed by epithelial cells, endothelial cells, and immune cells in the lung. In this mini-review, we discuss the anti-inflammatory mechanisms of adiponectin in lung cells and tissues.

Keywords: COPD; adiponectin; adiponectin receptors; asthma; infectious lung disease; inflammatory pulmonary disease; lung immune response; obesity.

Figure 1

Adiponectin effect on lung disease. Obesity and aging are associated with loss of muscle mass, insulin resistance, and features of metabolic syndromes. Adiponectin (APN) activity is linked to metabolism and inhibition of inflammation. Decreases/deficiencies in plasma APN, even due to obesity, may contribute to adipose tissue inflammation, induction of asthma and TNF-α production in adipose and non-adipose tissues such as the lung. APN regulates inflammation in chronic pulmonary disease (COPD), asthma, fungal, bacterial, and viral infection. Adiponectin deficiency in COPD, aspergillosis, viral infection or tuberculosis resulted in increased expression of the proinflammatory cytokines TNF-α and IL-6, further suggesting that APN functions exerts anti-inflammatory activity. However, the effects of APN or AdipoRon on viral infection remain unknown. Treatment with APN or its agonist affects cytokine production; a decrease of IL-13 and IL-5 in asthma model and an increase of IL-8 in COPD, and increased IL-4, 1L-17, IL-23, and TNF-α in asthma. APN treatment also inhibited lung eosinophil recruitment in response to chitin.