Sodium arsenite induces the stress response in the gut and decreases bacterial translocation in a burned mouse model with gut-derived sepsis

Bacteria translocation from the bowel to systemic organs after burn injury may contribute to or be a cause of sepsis and multiple organ failure. The s tress response confers protection under stressful conditions that would oth erwise lead to cell damage or death. We investigated whether prior inductio n of the stress response by sodium arsenite could affect bacterial transloc ation after thermal injury. HSP-70, a highly stress-inducible protein, was used as a marker for induction of the stress response. Balb/c mice were int ravenously injected with 4 mg/kg of sodium arsenite and killed at selected times past-treatment. Other treated mice were then gavaged with 10(10) E. c oil or 10(10) In-111-labeled E. coli followed by a 20% burn. Survival was o bserved for 10 days. Mice gavaged with radiolabeled E, coil were killed 4 h post-burn to determine the effect of HSP-70 induction on microbial translo cation in mesenteric lymph nodes (MLN), liver, and spleen. Sodium arsenite- injected mice showed HSP-70 induction in the ileum that Increased in a time -dependent manner with peak expression 12 h post-injection. Treated mice sh owed a significantly higher survival rate (93%) than controls (46%; P <:0.0 5), and detection of In-111-labeled E, coli was significantly less in the l iver and spleen (P < 0.05). These data show that sodium arsenite induced HS P-70 expression In the small intestine. The stress response was associated with significantly increased survival and significant decrease in detection of In-111-labeled E. coli in the liver and spleen in a burned mouse model with gut-derived sepsis.