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 stress response confers protection under stressful conditions that would otherwise lead to cell damage or death. We investigated whether prior induction of the stress response by sodium arsenite could affect bacterial translocation 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 intravenously injected with 4 mg/kg of sodium arsenite and killed at selected times post-treatment. Other treated mice were then gavaged with 10¹⁰ E. coli or 10^{10 111}In-labeled E. coli followed by a 20% burn. Survival was observed for 10 days. Mice gavaged with radiolabeled E. coli were killed 4 h post-burn to determine the effect of HSP-70 induction on microbial translocation 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 showed a significantly higher survival rate (93%) than controls (46%; P < 0.05), and detection of ¹¹¹ln-labeled E. coli was significantly less in the liver and spleen (P < 0.05). These data show that sodium arsenite induced HSP-70 expression in the small intestine. The stress response was associated with significantly increased survival and significant decrease in detection of ¹¹¹In-labeled E. coli in the liver and spleen in a burned mouse model with gut-derived sepsis.