AIM:To determine whether Carbon (CO) liberated from CO-releasing molecules attenuates leukocyte infiltration in the small intestine of thermally injured mice. METHODS:Thirty-six mice were assigned to four groups. Mice in the sham group (n=9) were underwent to sham thermal injury;mice in the burn group (n=9) received 15% total body surface area full-thickness thermal injury;mice in the burn+CORM-2 group (n=9) were underwent to the same thermal injury with immediate administration of tricarbonyldichlororut henium (Ⅱ) dimer CORM-2 (8 mg/kg,i.v.);and mice in the burn+DMSO group (n=9) were underwent to the same thermal injury with immediate administration of 160μL bolus injection of 0.5% DMSO/saline.Histological alterations and granulocyte infiltration of the small intestine were assessed.Polymorphonuclear neutrophil (PMN) accumulation (myeloperoxidase assay) was assessed in mice mid-ileum.Activation of nuclear factor (NF)-κB,expression levels of intercellular adhesion molecule-1 (ICAM-1) and inducible heme oxygenase in mid-ileum were assessed. RESULTS:Treatment of thermally injured mice with CORM-2 attenuated PMN accumulation and prevented activation of NF-κB in the small intestine.This was accompanied by a decrease in the expression of ICAM-1. In parallel,burn-induced granulocyte infiltration in mid- ileum was markedly decreased in the burn mice treated with CORM-2. CONCLUSION:CORM-released CO attenuates leukocyte infiltration in the small intestine of thermally injured mice by interfering with NF-κB activation and protein expression of ICAM-1,and therefore suppressing the pro-adhesive phenotype of endothelial cells. AIM: To determine whether Carbon (CO) liberated from CO-releasing molecules attenuates leukocyte infiltration in the small intestine of thermally injured mice. METHODS: Thirty-six mice were assigned to four groups. Mice in the sham group (n = 9) were underwent to sham thermal injury; mice in the burn group (n = 9) received 15% total body surface area full-thickness thermal injury; mice in the burn + CORM-2 group (n = 9) were underwent to the same thermal injury with immediate administration of tricarbonyldichlororut henium (II) dimer CORM-2 (8 mg / kg, iv); and mice in the burn plus DMSO group (n = 9) were underwent to the same thermal injury with immediate administration of 160 μL bolus injection of 0.5% DMSO / saline. Histological alterations and granulocyte infiltration of the small intestine were assessed. Polymorphonuclear neutrophil (PMN) accumulation (myeloperoxidase assay) was assessed in mice mid-ileum. Activation of nuclear factor adhesion molecule-1 (ICAM- 1) and inducible heme oxygenase in mid-ileum were assessed. RESULTS: Treatment of thermally injured mice with CORM-2 attenuated PMN accumulation and prevented activation of NF-κB in the small intestine. This was accompanied by a decrease in the expression of ICAM -1. In parallel, burn-induced granulocyte infiltration in mid-ileum was markedly decreased in the burn mice treated with CORM-2. CONCLUSION: CORM-released CO attenuates leukocyte infiltration in the small intestine of thermally injured mice by interfering with NF- κB activation and protein expression of ICAM-1, and suppress the pro-adhesive phenotype of endothelial cells.