title: Bacterial translocation in small intestinal ischemia-reperfusion injury and efficacy of Anti-CINC antibody treatment.
abstract: The involvement of bacterial translocation in small intestinal ischemia-reperfusion injuries and the efficacy of using anti-CINC antibodies for treatment were investigated. A model for ischemia-reperfusion injury of the small intestine was constructed by clamping the supramesenteric artery (for 90 min) in rats. Anti-CINC antibodies and saline were given just before the induction of ischemia in the treatment group and the control group, respectively. Six hours after reperfusion, bacteria were detected in the mesenteric lymph nodes, but the 'bacteria-positive' rate was significantly lower in the treatment group than in the control group. Bacterial cultures and endotoxins in the blood were negative in both groups up to 24 h later. The plasma cytokine levels showed similar variations, although the increases were significantly lower after reperfusion in the treatment group. In addition, the degrees of neutrophil infiltration and mucosal injury were attenuated in the small intestine, and the structure of the liver was maintained. Furthermore, the 1-week survival was improved. These results suggest that bacterial translocation occurred predominantly via the lymphatic system and that anti-CINC antibody treatment exerted a protective effect against small intestinal ischemia-reperfusion injury.
authors.affiliation: Department of Surgery, Omori Hospital, Toho University, Tokyo, Japan. hironori@med.toho-u.ac.jp
authors.forename: H
authors.initials: H
authors.lastname: Kaneko
authors.forename: A
authors.initials: A
authors.lastname: Tamura
authors.forename: T
authors.initials: T
authors.lastname: Ishii
authors.forename: T
authors.initials: T
authors.lastname: Maeda
authors.forename: T
authors.initials: T
authors.lastname: Katagiri
authors.forename: J
authors.initials: J
authors.lastname: Ishii
authors.forename: Y
authors.initials: Y
authors.lastname: Kubota
authors.forename: T
authors.initials: T
authors.lastname: Suzuki
authors.forename: M
authors.initials: M
authors.lastname: Tsuchiya
authors.forename: Y
authors.initials: Y
authors.lastname: Otsuka
authors.forename: K
authors.initials: K
authors.lastname: Yamazaki
authors.forename: M
authors.initials: M
authors.lastname: Watanabe
authors.forename: T
authors.initials: T
authors.lastname: Tatsuo
mesh_terms: D000818:Animals; D000906:Antibodies / Q000627:therapeutic use; D018988:Bacterial Translocation / Q000502:physiology*; D054360:Chemokine CXCL1; D019743:Chemokines, CXC / Q000276:immunology*; D016207:Cytokines / Q000097:blood; D004731:Endotoxins / Q000097:blood; D013293:Enterococcus faecalis; D004926:Escherichia coli; D007421:Intestine, Small / Q000382:microbiology / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D020613:Morganella morganii; D018375:Neutrophil Activation / Q000502:physiology*; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000188:drug therapy / Q000382:microbiology / Q000503:physiopathology*
chemical_list: D000906:Antibodies; D054360:Chemokine CXCL1; D019743:Chemokines, CXC; C513297:Cxcl1 protein, rat; D016207:Cytokines; D004731:Endotoxins; D009195:Peroxidase