From acinar cell damage to systemic inflammatory response: current concepts in pancreatitis.
Acute pancreatitis represents a local inflammatory disorder with severe systemic consequences. Significant progress in understanding the pathophysiology of acute pancreatitis has been achieved in recent years. However, there is no clear concept about initialization and propagation of the disease both in experimental models and in humans. Furthermore, reliable strategies to evaluate prognosis and perform therapy are still missing. The review focuses on mechanisms originating from acinar cells leading to a systemic inflammatory response in experimental pancreatitis.
Department of Medicine I, University of Ulm, Robert-Koch-Strasse 8, D-89081 Ulm, Germany.
C K
CK
Weber
G
G
Adler
D000818:Animals; D002118:Calcium / Q000502:physiology; D003599:Cytoskeleton / Q000473:pathology; D006801:Humans; D007111:Immunity, Cellular / Q000502:physiology; D018836:Inflammation Mediators / Q000502:physiology; D016328:NF-kappa B / Q000502:physiology; D010195:Pancreatitis / Q000201:enzymology / Q000276:immunology / Q000473:pathology* / Q000503:physiopathology; D014357:Trypsin / Q000502:physiology
D018836:Inflammation Mediators; D016328:NF-kappa B; D014357:Trypsin; D002118:Calcium