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- Title
IL-15 protects intestinal epithelial cells.
- Authors
Obermeier, Florian; Hausmann, Martin; Kellermeier, Silvia; Kiessling, Stefan; Strauch, Ulrike G.; Duitman, Erwin; Bulfone-Paus, Silvia; Herfarth, Hans; Bock, Jürgen; Dunger, Nadja; Stoeck, Michael; Schölmerich, Jürgen; Falk, Werner; Rogler, Gerhard
- Abstract
IL-15, a T-cell growth factor, has been shown to be increased in inflammatory bowel disease (IBD). It has been suggested that neutralization of IL-15 could protect from T cell-dependent autoimmune inflammation. On the other hand, an anti-apoptotic effect of IL-15 has been demonstrated in kidney epithelial cells during nephritis. We therefore tested the role of IL-15 in two different experimental models of colitis in vivo, and in models of intestinal epithelial cell (IEC) apoptosis in vitro. IL-15 blockade in chronic dextran sulphate sodium-induced colitis resulted in aggravation of the disease with a significantly 2.1-fold increased epithelial damage score compared to controls. TUNEL staining clearly revealed increased apoptosis. IL-6, TNF and IFN-γ secretion by mesenteric lymph node cells were increased. In the T cell-dependent SCID transfer model of colitis IL-15 neutralization reduced the inflammatory infiltration and proinflammatory cytokine production. Despite that, the intestinal epithelial damage was not reduced. In vitro, IL-15 pre-incubation prevented up to 75% of CH11 antibody-induced apoptosis in SW-480 cells and reduced caspase-3 activity. According to this, endogenously produced IL-15 in chronic colitis does not only act as a proinflammatory cytokine but has at the same time the potential to reduce mucosal damage by preventing IEC apoptosis.
- Publication
European Journal of Immunology, 2006, Vol 36, Issue 10, p2691
- ISSN
0014-2980
- Publication type
Article
- DOI
10.1002/eji.200535173