title: Prevention of small intestinal ischemia-reperfusion injury in rat by anti-cytokine-induced neutrophil chemoattractant monoclonal antibody.
abstract: The function of cytokine-induced neutrophil chemoattractant (CINC), which is the rat counterpart to human growth-related gene product belonging to the CXC chemokine subgroup, is based principally on neutrophil-specific chemotactic activity. In addition, we previously reported that plasma CINC was elevated during the period of small intestinal ischemia-reperfusion injury, and that there was a correlation between the degree of mucosal damage and the peak level of CINC after reperfusion, suggesting that CINC may play a major role in neutrophil infiltration into the rat small intestinal ischemia-reperfusion injury site. Thus, we investigated whether administration of anti-CINC monoclonal antibodies (mAbs) reduces small intestinal ischemia-reperfusion injury. Small intestine was subjected to ischemia for 3 h by occlusion of the anterior mesenteric artery with an atraumatic vascular clump. After infusion of anti-CINC mAbs or isotype-matched mAbs, the intestine was subjected to reperfusion. The pretreatment with anti-CINC mAbs attenuated ischemia-reperfusion injury in the small intestine, in association with the reduction of tumor necrosis factor-alpha and myeloperoxidase production, and resulted in the prolongation of survival. It is concluded that CINC plays an important role in the onset of rat small intestinal ischemia-reperfusion injury. In addition, blocking the action of CINC, namely, the neutrophil chemotactic activity, may be useful in preventing ischemia-reperfusion injury in the small intestine.
authors.affiliation: Department of Surgery, Department of Laboratory Diagnosis, Sapporo Medical University School of Medicine, South-1, West-16, Chuo-ku, Sapporo, 060-0061, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Yagihashi
authors.forename: T
authors.initials: T
authors.lastname: Tsuruma
authors.forename: K
authors.initials: K
authors.lastname: Tarumi
authors.forename: T
authors.initials: T
authors.lastname: Kameshima
authors.forename: T
authors.initials: T
authors.lastname: Yajima
authors.forename: Y
authors.initials: Y
authors.lastname: Yanai
authors.forename: N
authors.initials: N
authors.lastname: Watanabe
authors.forename: K
authors.initials: K
authors.lastname: Hirata
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology*; D054360:Chemokine CXCL1; D019743:Chemokines, CXC; D002630:Chemotactic Factors / Q000276:immunology*; D006131:Growth Inhibitors / Q000276:immunology*; D006133:Growth Substances / Q000276:immunology*; D036341:Intercellular Signaling Peptides and Proteins; D007413:Intestinal Mucosa / Q000098:blood supply / Q000201:enzymology / Q000276:immunology; D007421:Intestine, Small / Q000098:blood supply* / Q000201:enzymology / Q000276:immunology; D007511:Ischemia / Q000276:immunology / Q000401:mortality / Q000517:prevention & control*; D008026:Ligation; D008297:Male; D008638:Mesenteric Arteries / Q000601:surgery; D009195:Peroxidase / Q000096:biosynthesis; D051381:Rats; D011917:Rats, Inbred Lew; D015427:Reperfusion Injury / Q000276:immunology / Q000401:mortality / Q000517:prevention & control*; D016019:Survival Analysis; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
chemical_list: D000911:Antibodies, Monoclonal; C475829:CXCL1 protein, human; D054360:Chemokine CXCL1; D019743:Chemokines, CXC; D002630:Chemotactic Factors; C513297:Cxcl1 protein, rat; D006131:Growth Inhibitors; D006133:Growth Substances; D036341:Intercellular Signaling Peptides and Proteins; D014409:Tumor Necrosis Factor-alpha; D009195:Peroxidase