T. Eaves-pyles et al., Sodium arsenite induces the stress response in the gut and decreases bacterial translocation in a burned mouse model with gut-derived sepsis, SHOCK, 13(4), 2000, pp. 314-319
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.