Figure 2.

Roles of IL-17 in acute pancreatitis. Etiology for AP include gallstones, alcohol and hypertriglyceridemia, which cause pathophysiological changes of AP. IL-17A induce pancreatic acinar cell damage through synthesizing and releasing cytokines and chemokines which recruit immune cells, such as neutrophils and macrophages. IL-17 also directly induce chemokines and activate innate immune cells, releasing pro-inflammatory mediators. Different inflammatory factors act in synergy with each other to aggravate AP. Furthermore, the intestinal microbiota-derived signals to IL-17 include microbiota alteration, bacteria-derived metabolites and impaired intestinal barrier function. Systemic injury develops early due to IL-17 involving inflammatory response and may precede necrosis, and late secondary organ failure due to infected pancreatic necrosis (IPN) induce sepsis.