Neutrophil depletion in rats reduces burn-injury induced intestinal bacterial translocation

Objective: To determine whether neutrophil depletion could eradicate intest inal bacterial translocation in burn-injured rats. Design: Prospective, randomized, controlled study. Setting: University research laboratory. Subjects: Adult male Sprague-Dawley rats. Interventions: The rats were intravenously administered a rabbit anti-rat;n eutrophil antibody causing profound neutropenia and subjected to a 30% tota l body surface area scald burn. Measurements and Main Results: The depletion of neutrophils from-the intest ine was assessed via measurements of myeloperoxidase (MPO) activity in the intestinal homogenates. In addition, the presence of activated/extravasated neutrophils in intact intestines was determined via immunohistochemical lo calization of neutrophil nicotinamide adenine dinucleotide phosphate (NADPH ) oxidase component protein p47phox, Bacterial translocation was measured u sing agar cultures and by determining Escherichia coli beta-galactosidase g ene via polymerase chain reaction/Southern blot analyses of mesenteric lymp h node and spleen, liver, lung, and blood. MPO measurements demonstrated a six-fold increase above the control value in the intestinal tissue in rats on day 1 postburn, The presence of activated neutrophils (expression of p47 phox protein) was also markedly increased in the intestines of these rats. The increased MPO activity and p47phox expression accompanied a translocati on of indigenous E. coli into the mesenteric lymph node without a spread to other organs. The administration of anti-neutrophil antibody to burn anima ls prevented an increase in MPO activity and bacterial translocation. Conclusion: These studies indicate that enhanced intestinal bacterial trans location caused by burn injury could be related to the increased infiltrati on of activated neutrophils into the intestinal tissue after burn, The rele ase of neutrophil products such as superoxide anion may effect intestinal t issue damage leading to bacterial translocation of indigenous E. coli.