Genetic susceptibility to mucosal damage leads to bacterial translocation in a murine burn model

Since genetic factors may be important in host resistance to infections after thermal injury, we screened the susceptibility of three mouse strains (CD-1, Balb/c, and C57/bl) to thermally induced bacterial translocation from the GI tract. Bacteria translocated to the MLNs of Balb/c but not the CD-1 or C57/bl mice receiving 25% body burns. The increased incidence of bacterial translocation in the burned Balb/c mice appeared to be due to a burn-induced gut mucosal injury, since the intestinal mucosa of the Balb/c but not the CD-1 or C57/bl mice was damaged 24 hr after the thermal injury. The mucosal injury appears to be mediated, at least in part, by xanthine oxidase-generated oxygen-free radicals, since inhibition of xanthine oxidase activity with allopurinol, or inactivation of xanthine oxidase activity by a molybdenum-free tungsten diet, prevented the mucosal injury and reduced the extent of bacterial translocation.