期刊
FREE RADICAL BIOLOGY AND MEDICINE
卷 51, 期 10, 页码 1903-1909出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2011.08.026
关键词
Oxidized phospholipids; Inflammation; Toll-like receptor; Macrophage; Free radicals
资金
- NIH [R01 HL-084422]
- Max Kade postdoctoral fellowship
- AHA postdoctoral fellowship
Oxidative tissue damage is a hallmark of many chronic inflammatory diseases. However, the precise mechanisms linking oxidative changes to inflammatory reactions remain unclear. Herein we show that Toll-like receptor 2 (TLR2) translates oxidative tissue damage into inflammatory responses by mediating the effects of oxidized phospholipids. Intraperitoneal injection of oxidized 1-palmitoy1-2-arachidonyl-sn-3-glycerophosphorylcholine (OxPAPC) resulted in upregulation of inflammatory genes in wild-type, but not in TLR2(-/-) mice. In vitro, OxPAPC induced TLR2 (but not TLR4)-dependent inflammatory gene expression and JNK and p38 signaling in macrophages. Induction of TLR2-dependent gene expression required reducible functional groups on sii-2 acyl chains of oxidized phospholipids, as well as serum cofactors. Finally, TLR2(-/-) - mice were protected against carbon tetrachloride-induced oxidative tissue damage and inflammation, which was accompanied by accumulation of oxidized phospholipids in livers. Together, our findings demonstrate that TLR2 mediates cellular responses to oxidative tissue damage and they provide new insights into how oxidative stress is linked to acute and chronic inflammation. (C) 2011 Elsevier Inc. All rights reserved.
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