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Release of inflammatory mediators by adipose tissue during acute pancreatitis

AuthorsFranco-Pons, Neus ; Gea-Sorlí, Sabrina ; Closa, Daniel
Issue Date2010
CitationJournal of Pathology 221(2): 175-182 (2010)
AbstractObesity and lipid metabolism are associated with the severity of acute pancreatitis. Fat necrosis appears in the severe acute pancreatitis as a consequence of the release of lipolytic enzymes, but its potential role on the progression of the disease is unclear. In this study, we have examined the role of white adipose tissue as a source of inflammatory mediators that can promote systemic inflammation during experimental taurocholate-induced acute pancreatitis in rats. The inflammatory status and the expression of TNFα, iNOS, adiponectin and IL-10 were determined in necrotic and non-necrotic areas of adipose tissue. Samples of adipose tissue were also used to induce the activation of macrophages in vitro. Finally, the release of TNFα to mesenterial vessels surrounded by necrotic or non-necrotic fat was evaluated in ex vivo perfused mesenterium. A strong inflammatory infiltrate was observed in the border between necrotic and non-necrotic areas of adipose tissue. In these areas, high expression of TNFα and iNOS and a reduced expression of IL-10 were observed, while adiponectin showed only a moderate increase. Necrotic fat strongly activates peritoneal macrophages in vitro. Mesenterial areas with fat necrosis release to the vascular vessels significantly increased amounts of TNFα when compared to vessels without necrosis. Altogether, these results indicate that adipose tissue inflammation is a process secondary to acute pancreatitis but also contributes to the generation of mediators potentially involved in the induction of the systemic inflammatory response. In particular, the areas of fat necrosis are important sources of inflammatory mediators. Copyright © 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Publisher version (URL)http://dx.doi.org/10.1002/path.2691
Identifiersdoi: 10.1002/path.2691
issn: 0022-3417
e-issn: 1096-9896
Appears in Collections:(IIBB) Artículos
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