Adiponectin and adiponection receptor 1 enhance colon inflammation (902.8)

Abstract

Adiponectin (ADN) is an adipokine derived from adipocytes. It binds to adiponectin recetor1 and 2 (AdipoR1 and 2) to exert into function regulating in whole‐body energy homeostasis, anti‐cardiovascular disease and inflammatory response. The role of ADN in inflammation response is likely multifaceted. We established the murine colitis model. After administration of 2% DSS in drinking water for 7 days, AdipoR1‐transgenic mice developed more severe colitis than wild‐type mice, the symptoms including body weight loss, bloody‐diarrhea, short colon length, crypt disruption and immunity cell infiltration. We also administrated ADN to THP‐1 cell (monocyte cell line) and HT29 cell (colon epithelial cell line). In colon epithelial cell, ADN does not enhance the expression of pro‐inflammatory factor (TNFα, IL‐1 and IL‐6) and inducible cyclooxygenase 2/cox2) but chemokine (IL‐8). However, ADN increased cox2 and IL‐8 expression in the inflammatory state. In macrophage ADN increased the pro‐inflammatory cytokine (TNFα) and chemokine (IL‐8). ADN increase the expression of IL‐1 in cell inflammatory state. In macrophage, ADN does not affect cox2 expression. ADN decreased cox2 expression and increase IL‐1 expression in the inflammatory state. Our data show that ADN may play a pro‐inflammatory role in colitis by increasing pro‐inflammatory cytokine and inducing immune cell infiltration.