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Updated: Jun 15, 2026
Murine Model of Intestinal Ischemia-reperfusion Injury
Published on: May 11, 2016
Decay-accelerating factor attenuates C-reactive protein-potentiated tissue injury after mesenteric
Xinyue Lu1, Yansong Li, Milomir O Simovic
1Division of Military Casualty Research, Walter Reed Army Institute of Research, Silver Spring, Maryland, USA.
Background:
C-reactive protein (CRP) is an acute pro-inflammatory mediator that has been demonstrated to enhance ischemia/reperfusion (IR) injury by virtue of activating the complement system. CRP is able to interact with complement proteins such as C1q, complement factor H, and C4b-binding protein. Since complement activation is central in the expression of tissue injury following IR, we have investigated the effects of human decay-accelerating factor (DAF), a complement inhibitor, on CRP-potentiated complement activation and tissue injury in mice subjected to mesenteric IR.
Materials And Methods:
Male C57B1/6 mice were allocated into eight groups: (1) Sham-operated group without IR injury; (2) CRP+Sham group; (3) IR group; (4) CRP+IR group; (5) DAF group; (6) CRP+DAF group; (7) IR+DAF group, and (8) CRP+IR+DAF group. Intestinal and lung injury, neutrophil infiltration, myeloperoxidase (MPO) expression, complement component deposition, and interleukin-6 (IL-6) production were assessed for each treatment group of mice.
Results:
We report that administration of DAF significantly attenuates the CRP-enhanced intestinal injury as well as remote lung damages following acute mesenteric IR in mice, while DAF inhibits complement activation, suppresses neutrophil infiltration, and reduces IL-6 production.
Conclusions:
Our study suggests that inhibition complement activation with DAF may prove useful for the treatment of post-ischemic inflammatory injuries associated with an increased production of CRP.
