Journal of Neuroinflammation | |
Toll-like receptors in cerebral ischemic inflammatory injury | |
Qing-Wu Yang1  Sen Lin2  Yan-Chun Wang1  | |
[1] Department of Neurology, Daping Hospital, Third Military Medical University, Changjiang Branch Road No. 10, Yuzhong District, Chongqing 400042, PR China;Development and Regeneration Key Laboratory of Sichuan Province, Department of Histo-embryology and Neurobiology, Chengdu Medical College, Chengdu 610083, PR China | |
关键词: innate immunity; inflammation; Toll-like receptors (TLRs); cerebral ischemia; | |
Others : 1213072 DOI : 10.1186/1742-2094-8-134 |
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received in 2011-07-20, accepted in 2011-10-08, 发布年份 2011 | |
【 摘 要 】
Cerebral ischemia triggers acute inflammation, which has been associated with an increase in brain damage. The mechanisms that regulate the inflammatory response after cerebral ischemia are multifaceted. An important component of this response is the activation of the innate immune system. However, details of the role of the innate immune system within the complex array of mechanisms in cerebral ischemia remain unclear. There have been recent great strides in our understanding of the innate immune system, particularly in regard to the signaling mechanisms of Toll-like receptors (TLRs), whose primary role is the initial activation of immune cell responses. So far, few studies have examined the role of TLRs in cerebral ischemia. However, work with experimental models of ischemia suggests that TLRs are involved in the enhancement of cell damage following ischemia, and their absence is associated with lower infarct volumes. It may be possible that therapeutic targets could be designed to modulate activities of the innate immune system that would attenuate cerebral brain damage. Ischemic tolerance is a protective mechanism induced by a variety of preconditioning stimuli. Interpreting the molecular mechanism of ischemic tolerance will open investigative avenues into the treatment of cerebral ischemia. In this review, we discuss the critical role of TLRs in mediating cerebral ischemic injury. We also summarize evidence demonstrating that cerebral preconditioning downregulates pro-inflammatory TLR signaling, thus reducing the inflammation that exacerbates ischemic brain injury.
【 授权许可】
2011 Wang et al; licensee BioMed Central Ltd.
【 预 览 】
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Figure 1.
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