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Intestinal reperfusion injury is mediated by IgM and complement.
J P Williams1, T T Pechet, M R Weiser
1Department of Surgery, Harvard Medical School, and Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|March 6, 1999
Summary
Intestinal ischemia-reperfusion injury relies on the classic complement pathway and IgM. Blocking these pathways significantly reduced injury in a mouse model, highlighting their critical role.
Area of Science:
- Immunology
- Gastroenterology
- Pathophysiology
Background:
- Intestinal ischemia-reperfusion (I/R) injury is a significant clinical problem.
- The complement system plays a role in I/R injury, but specific pathway involvement is unclear.
Purpose of the Study:
- To investigate the roles of the alternative and classic complement pathways and immunoglobulin M (IgM) in intestinal I/R injury.
- To elucidate the mechanisms underlying complement activation in this context.
Main Methods:
- Utilized a murine model of jejunal ischemia (40 min) and reperfusion (3 h).
- Compared wild-type mice with knockout mice (deficient in complement factor 4 (C4), C3, or Ig) and wild-type mice treated with soluble complement receptor 1.
- Assessed intestinal injury by measuring permeability to radiolabeled albumin and performed immunohistological staining for C3 and IgM.
Main Results:
- Mice deficient in C4, C3, or Ig, as well as those treated with soluble complement receptor 1, exhibited significantly reduced intestinal injury compared to wild-type controls.
- Reconstitution of Ig-deficient mice with IgM restored the injury levels to those seen in wild-type animals.
- Immunohistology revealed colocalization of C3 and IgM in the mucosa of wild-type mice, with minimal staining in Ig-deficient and C4-deficient mice.
Conclusions:
- Intestinal I/R injury is critically dependent on the classic complement pathway.
- IgM is essential for mediating complement-dependent intestinal I/R injury.