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 b group (n = 9)received 15% total body surface area full-thickness thermal injury; mice in the b + 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 b+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 (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, b-induced granulocyte infiltration in midileum was markedly decreased in the b 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.