Caerulein induced pancreatitis

• Published in: Gut Vol. 52; no. 3; pp. 452 - 453
• Main Authors: van Westerloo, D J, Maris, N A, Bruno, M J, van der Poll, T
• Format: Journal Article
• Language: English
• Published: England BMJ Publishing Group Ltd and British Society of Gastroenterology 01.03.2003; BMJ Publishing Group LTD; BMJ Group
• Subjects: Acute Disease; Animals; Bacterial Proteins; caerulein; Catecholamines - physiology; Ceruletide - toxicity; Chaperonin 60; Chaperonins - physiology; Cytokines; Gangrene; Heat shock proteins; Letter; Neutrophils; Pancreas; pancreatitis; Pancreatitis - chemically induced; Rodents; Studies; thermal stress; trypsinogen; Tumor necrosis factor-TNF
• ISSN: 0017-5749; 1468-3288
• DOI: 10.1136/gut.52.3.452-a

[...]catecholamines exert anti-inflammatory effects on the cytokine network by inhibiting the production of proinflammatory cytokines such as tumour necrosis factor (TNF), interleukin (IL)-1β, IL-12, and interferon [GAMMA] (IFN-[GAMMA]), of which TNF and IL-1β have been implicated as mediators that play a proinflammatory role in acute pancreatitis. 3, 4 Secondly, in animal models of endotoxaemia, pretreatment with isoproterenol enhances the production of the anti-inflammatory cytokine IL-10 which has been shown to be protective in acute pancreatitis. 5, 6 Thirdly, in endotoxaemia models, β adrenergic stimulation results in reduction of levels of CC chemokines. 7 Fourthly, neutrophil migration to the pancreas, one of the hallmarks of acute pancreatitis, towards chemotactic stimuli such as C5a and lipopolysaccharide (LPS) is reduced by administration of β agonists but also affects LPS induced neutrophil degranulation in vivo.