Fichtner-Feigl, Stefan and Kesselring, Rebecca and Martin, Maria and Obermeier, Florian and Ruemmele, Petra and Kitani, Atsushi and Brunner, Stefan M. and Haimerl, Michael and Geissler, Edward K. and Strober, Warren and Schlitt, Hans J. (2014) IL-13 Orchestrates Resolution of Chronic Intestinal Inflammation via Phosphorylation of Glycogen Synthase Kinase-3 beta. JOURNAL OF IMMUNOLOGY, 192 (8). pp. 3969-3980. ISSN 0022-1767, 1550-6606
Full text not available from this repository. (Request a copy)Abstract
Spontaneous amelioration of inflammation (often accompanied by fibrosis) is a well-known, but poorly understood, outcome of many chronic inflammatory processes. We studied this phenomenon in a chronic trinitrobenzene sulfonic acid-induced colitis model, an experimental colitis in mice that we showed to ultimately undergo spontaneous resolution, despite continued trinitrobenzene sulfonic acid stimulation. Analysis of the mechanism of this resolution revealed that it was critically dependent on IL-13 activation of STAT6, followed by phosphorylation (inactivation) of glycogen synthase kinase-3 delta, at least in part via STAT6 induction of p38 MAPK. Such glycogen synthase kinase-3 delta inactivation causes changes in CREB and p65 DNA-binding activity that favors decreased proinflammatory IL-17 production and increased anti-inflammatory IL-10 production. Thus, in this case, IL-13 acts as a molecular switch that leads to resolution of inflammation.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | ESTABLISHED EXPERIMENTAL COLITIS; TOLL-LIKE RECEPTOR; PROTEIN-KINASE; BOWEL-DISEASE; MURINE MODEL; INDUCTION; FIBROSIS; CELLS; GSK3; ANTIBODIES; |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Chirurgie Medicine > Lehrstuhl für Innere Medizin I Medicine > Lehrstuhl für Pathologie Medicine > Regensburger Centrum für Interventionelle Immunologie (RCI) |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 14 Nov 2019 09:54 |
| Last Modified: | 14 Nov 2019 09:54 |
| URI: | https://pred.uni-regensburg.de/id/eprint/10312 |
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