C5a causes limited, polymorphonuclear cell-independent, mesenteric ischemia/reperfusion-induced injury

C5a causes limited, polymorphonuclear cell-independent, mesenteric ischemia/reperfusion-induced injury
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DOI:
10.1016/s1521-6616(03)00160-8
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发表时间:
2003-09-01
影响因子:
8.6
通讯作者:
Tsokos, GC
Tsokos, GC
中科院分区:
医学3区
文献类型:
--
作者:
Fleming, SD;Mastellos, D;Tsokos, GC

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C5在肠系膜缺血/再灌注(IR)后局部粘膜损伤和炎症的发展以及远端器官损伤的发展中至关重要。为了确定C5 a在组织损伤中的作用,我们用环状六肽C5 a受体拮抗剂(C5 aRa)处理野生型小鼠,并将重组C5 a施用给经历肠系膜IR的C5缺陷(C5(-/-))小鼠。C5 a给予C5(-/-)IR期间的小鼠引起有限的肠粘膜损伤,但未引起远端肺损伤,尽管它上调了粘附分子表情经历IR的C5+/+小鼠的C5 aRa治疗限制了局部损伤并防止了远端器官损伤。我们的结论是,虽然C5 a可以触发某些成分的IR诱导的损伤,其他介质,如C5 b-9和局部因素是需要的IR组织损伤的完整表达。(C)2003年爱思唯尔公司All rights reserved.
C5 is critical in the development of local mucosal damage and inflammation as well as in the development of remote organ injury after mesenteric ischemia/reperfusion (IR). To define the role of C5a in tissue injury, we treated wild-type mice with a cyclic hexapeptide C5a receptor antagonist (C5aRa) and administered recombinant C5a to C5 deficient (C5(-/-)) mice subjected to mesenteric IR. We demonstrate that at 2-h postreperfusion, C5a administered to C5(-/-) mice during IR induces limited intestinal mucosal injury but failed to cause remote lung injury despite the fact that it upregulated adhesion molecule expression. C5aRa treatment of C5+/+ mice undergoing IR limited local injury and prevented distant organ injury. We conclude that although C5a can trigger certain components of the IR induced injury, other mediators such as C5b-9 and local factors are needed for the complete expression of IR tissue damage. (C) 2003 Elsevier Inc. All rights reserved.