A Novel Inhibitor of the Alternative Pathway of Complement Attenuates Intestinal Ischemia/Reperfusion-Induced Injury

被引:29
作者
Chen, Jie [1 ]
Crispin, Jose C. [1 ]
Lucca, Jurandir Dalle [2 ]
Tsokos, George C. [1 ]
机构
[1] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Div Rheumatol, Boston, MA 02115 USA
[2] Walter Reed Army Inst Res, Dept Cellular Injury, Silver Spring, MD USA
关键词
ischemia/reperfusion injury; CRIg-Fc; complement; alternative pathway; NATURAL ANTIBODIES; REPERFUSION INJURY; TISSUE-INJURY; AUTOANTIBODIES; CRIG;
D O I
10.1016/j.jss.2009.05.041
中图分类号
R61 [外科手术学];
学科分类号
摘要
Complement activation has been demonstrated to contribute significantly to the expression of IR-induced tissue damage. Each of the three complement pathways, classic, alternative, and lectin, has been implicated in the instigation of tissue pathology. In this study, we used a selective inhibitor of the alternative pathway, that is, a soluble form of complement receptor of the immunoglobulin superfamily (CRIg-Fc) to determine whether it can prevent IR tissue injury. We demonstrate that treatment of C57B1/6 mice prior to mesenteric IR prevents local (intestinal) and remote (lung) injury by limiting deposition of complement and entry of polymorphonuclear cells to the sites of injury. Our results show that CRIg-Fc represents a candidate to limit IR injury as it occurs in various clinical conditions. (C) 2011 Elsevier Inc. All rights reserved.
引用
收藏
页码:E131 / E136
页数:6
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