Abstract
Pro-inflammatory cytokines, such as TNF-α, IL-6 and IL-1β, and chemokines such as MCP-1, derived from stimulated acini, play a key role in the pathology of acute pancreatitis. Acinar cell destruction also results in activation and infiltration of inflammatory cells which release pro-inflammatory cytokines, and excessive production of cytokines leads to a systemic inflammatory response and multiple organ failure. Understanding the underlying roles of inflammation-related transcription factors such as NF-κB and STAT3 in regulating the network of inflammatory systems in early phase of acute pancreatitis may be crucial for the development of new therapeutic targets.
