Regulation of interleukin-1 in acute brain injury

被引:72
作者
Brough, David [1 ]
Tyrrell, Pippa J. [2 ]
Allan, Stuart M. [1 ]
机构
[1] Univ Manchester, Fac Life Sci, Manchester M13 9PT, Lancs, England
[2] Univ Manchester, Salford Royal Hosp Fdn Trust, Fac Med & Human Sci, Brain Injury Res Grp,Sch Biomed, Salford M6 8HD, Lancs, England
基金
英国医学研究理事会; 英国惠康基金;
关键词
STERILE INFLAMMATORY RESPONSE; RESOLVING LIPID MEDIATORS; INNATE IMMUNE-RESPONSE; NLRP3; INFLAMMASOME; NALP3; ISCHEMIC-STROKE; CELL-DEATH; RECEPTOR ANTAGONIST; APOPTOTIC CELLS; NECROTIC CELLS;
D O I
10.1016/j.tips.2011.06.002
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Inflammation is a complex vascular response that has evolved to eliminate infection and to repair injured tissue. It is subject to tight regulatory control of its initiation and resolution. Failure of an inflammatory response to resolve has become recognised as a major contributor to the pathology of diverse diseases (including acute brain injuries). Interleukin-1 (IL-1) is a pro-inflammatory cytokine and key contributor to damage after acute brain injury. Understanding the regulation of IL-1 production is vital for the development of new drug targets and therapies. In recent years, there have been major advances in how we understand the resolution of inflammatory responses, and in how IL-1 is regulated after injury. Advances are summarised here in the context of addressing how dampening the inflammatory response and actions of IL-1 provides a strategy for reducing damage after acute brain injury such as stroke.
引用
收藏
页码:617 / 622
页数:6
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