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Related Experiment Video

Updated: Jul 3, 2026

Murine Model of Intestinal Ischemia-reperfusion Injury

Murine Model of Intestinal Ischemia-reperfusion Injury

Published on: May 11, 2016

Complement component C5a mediates hemorrhage-induced intestinal damage.

Sherry D Fleming¹, Lauren M Phillips, John D Lambris

¹Division of Biology, Kansas State University, Manhattan, Kansas 66506, USA. sdflemin@ksu.edu

The Journal of Surgical Research

|July 22, 2008

Summary

This summary is machine-generated.

Complement activation contributes to intestinal damage after hemorrhage. Inhibiting complement component 5a (C5a) protects against this injury, suggesting C5a as a therapeutic target for hemorrhage-associated inflammation.

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Fixed Volume or Fixed Pressure: A Murine Model of Hemorrhagic Shock

Fixed Volume or Fixed Pressure: A Murine Model of Hemorrhagic Shock

Published on: June 6, 2011

Area of Science:

Immunology
Gastroenterology
Trauma Research

Background:

Complement system activation is implicated in intestinal damage and inflammation during hemorrhage.
The precise mechanisms linking complement to hemorrhage-induced injury remain unclear, though complement inhibition affects hemodynamic changes.

Purpose of the Study:

To investigate the role of complement component 5 (C5) and its effector molecule C5a in the pathogenesis of intestinal injury following hemorrhage.
To evaluate the therapeutic potential of targeting the C5a pathway in a mouse model of hemorrhagic shock.

Main Methods:

Utilized C57Bl/6 wildtype, complement 5 deficient (C5-/-), and complement 5 sufficient (C5+/+) mice subjected to 25% blood loss.
Administered a C5a receptor antagonist (C5aRa) to C57Bl/6 mice post-hemorrhage.
Assessed intestinal injury scores, leukotriene B4, and myeloperoxidase production in all experimental groups.

Main Results:

Hemorrhage induced significant intestinal inflammation and tissue damage within 2 hours in wildtype mice.
C5 deficient mice exhibited significantly reduced intestinal tissue damage (injury score 0.36) compared to wildtype mice (injury score 2.89) after hemorrhage (P < 0.05).
Treatment with C5aRa markedly reduced intestinal injury (injury score 0.88), leukotriene B4, and myeloperoxidase levels in hemorrhaged mice compared to untreated controls (P < 0.05).

Conclusions:

Complement activation, specifically involving C5 and C5a, plays a critical role in the development of hemorrhage-induced intestinal tissue inflammation and damage.
Targeting the C5a pathway with antagonists offers a promising therapeutic strategy for mitigating injury associated with hemorrhagic shock.