期刊
CELLULAR IMMUNOLOGY
卷 259, 期 1, 页码 27-32出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.cellimm.2009.05.009
关键词
TLR-signaling; Intestinal inflammation; Mucosal immunity
资金
- Swedish Research council
- Swedish Cancer Society
- Sahlgrenska University Hospital Foundation for Clinical Research
- Goteborg Medical Society
- Lars Hierta Memorial foundation
- Swedish Society of Medicine
- Magnus Bergwall Foundation
- Royal Society of Arts and Science in Goteborg
- Assar Gabrielsson Foundation
- O.E. and Edla Johansson's Foundation
- Adlerberts Research Foundation
- Anders OttoSvird and Ulrika Eklunds Foundation
Toll-like receptor (TLR) signaling is important for the induction of pro-inflammatory cytokines and interferon (IFN)-inducible genes in response to bacterial and viral challenge. Interleukin-1 receptor-associated kinase-1 (IRAK-1) is a signaling kinase situated downstream of the adapter protein myeloid differentiation factor 88 (MyD88) in the TLR intracellular signaling cascade and is required for normal signal transduction through this pathway. We investigated the importance of IRAK-1 in intestinal inflammation by using the dextran sulfate sodium (DSS)-colitis model. We show that IRAK-1 deficient mice are protected against systemic signs of inflammation, i.e., weight loss and spleen enlargement compared to wild-type controls irrespective of gender. However, IRAK-1(-/y) males but not IRAK-1(-/-) females display significant protection against colitis and thymic atrophy compared to wild-type mice. Our results indicate a gender specific effect of IRAK-1 in the DSS-induced colitis, an interesting finding since the Irak-1 gene is located on the X-chromosome and several inflammatory diseases have a gender dependent incidence. (C) 2009 Elsevier Inc. All rights reserved.
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