Intestinal reperfusion injury is mediated by IgM and complement

Departments of 1  Surgery and 2  Pathology, Harvard Medical School, and Brigham and Women's Hospital, Boston, Massachusetts 02115 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 mu...

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Bibliographic Details
Published in:Journal of applied physiology (1985) 1999-03, Vol.86 (3), p.938-942
Main Authors: Williams, Julian P, Pechet, Taine T. V, Weiser, Martin R, Reid, Russell, Kobzik, Les, Moore, Francis D., Jr, Carroll, Michael C, Hechtman, Herbert B
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Blood
Complement C3 - deficiency
Complement C3 - genetics
Complement C3 - physiology
Complement C4 - deficiency
Complement C4 - genetics
Complement C4 - physiology
Complement System Proteins - deficiency
Complement System Proteins - genetics
Complement System Proteins - physiology
Digestive system
Edema - pathology
Gastroenterology. Liver. Pancreas. Abdomen
Genes, RAG-1 - genetics
Immunoenzyme Techniques
Immunoglobulin M - physiology
Injuries
Intestinal Diseases - immunology
Intestinal Diseases - pathology
Medical sciences
Mice
Mice, Knockout
Other diseases. Semiology
Proteins
Reperfusion Injury - immunology
Reperfusion Injury - pathology
Stomach. Duodenum. Small intestine. Colon. Rectum. Anus
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Summary:Departments of 1  Surgery and 2  Pathology, Harvard Medical School, and Brigham and Women's Hospital, Boston, Massachusetts 02115 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. immunoglobulin M; rodent; inflammation; complement; transgenic/knockout
ISSN:8750-7587
1522-1601
DOI:10.1152/jappl.1999.86.3.938