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.

Neutrophil priming by hypoxic preconditioning protects against epithelial barrier damage and enteric bacterial translocation in intestinal ischemia/reperfusion

“…These findings suggest that in addition to their bacterial-killing activity, neutrophils may also contribute to the process of epithelial restitution and maintenance of mucosal barrier integrity on ischemic challenge. Therefore, in contrast to the common belief that neutrophil activation is a cause for histopathology and barrier damage in ischemic intestines, 25,26,54 our findings suggest that neutrophils may be involved in protective mechanisms conferred by HPC to maintain gut barrier integrity. Previous studies of chemically induced colitis in rats revealed that depletion or adhesion blockade of neutrophils aggravated the intestinal histopathology, and promotion of bone marrow-derived granulocyte differentiation facilitated the mucosal repair processes.…”

Bacterial translocation and change in intestinal permeability in patients after abdominal surgery

“…The fact that the 5 patients with hypotension during operation yielded PCR-positive result supports such assumption. This pathophysiological phenomenon is attributable to visceral angiospasm induced by trauma and anesthesia, intestinal ischemia and anoxemia caused by blood loss, the production of vasoactive facotrs and prostaglandins [25][26][27] , ischemia-reperfusion injury [28] and the release of inflammatory cytokines [29] during abdominal surgery. Therefore, the improvement in surgical techniques, shortening of operation time, reduction in trauma and blood loss might be important in lessening BT.…”

Acute mesenteric ischemia after cardio-pulmonary bypass surgery

“…Several molecules have been identified which attenuate intestinal injury and reduce the production of proinflammatory cytokines [105][106][107][108][109][110] . Intra-luminal infusion of hyperoxygenated solution during ischemia may improve the functional and structural status of the enterocyte mitochondria associated with ischemia/reperfusion syndrome [111] .…”