Intestinal reperfusion injury is mediated by IgM and complement. Academic Article uri icon

Overview

abstract

  • Intestinal ischemia-reperfusion injury is dependent on complement. This study examines the role of the alternative and classic pathways of complement and IgM in a murine model of intestinal ischemia-reperfusion. Wild-type animals, mice deficient in complement factor 4 (C4), C3, or Ig, or wild-type mice treated with soluble complement receptor 1 were subjected to 40 min of jejunal ischemia and 3 h of reperfusion. Compared with wild types, knockout and treated mice had significantly reduced intestinal injury, indicated by lowered permeability to radiolabeled albumin. When animals deficient in Ig were reconstituted with IgM, the degree of injury was restored to wild-type levels. Immunohistological staining of intestine for C3 and IgM showed colocalization in the mucosa of wild-type controls and minimal staining for both in the intestine of Ig-deficient and C4-deficient mice. We conclude that intestinal ischemia-reperfusion injury is dependent on the classic complement pathway and IgM.

publication date

  • March 1, 1999

Research

keywords

  • Complement System Proteins
  • Immunoglobulin M
  • Intestinal Diseases
  • Reperfusion Injury

Identity

Scopus Document Identifier

  • 0033020662

Digital Object Identifier (DOI)

  • 10.1152/jappl.1999.86.3.938

PubMed ID

  • 10066708

Additional Document Info

volume

  • 86

issue

  • 3