Carbon liberated from CO-releasing molecules attenuates leukocyte infiltration in the small intestine of thermally injured mice

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 （11） 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 160 IJL 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）-KB, 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-kB 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 leukocyteinfiltration in the small intestine of thermally injured mice by interfering with NF-KB activation and protein expression of ICAM-1, and therefore suppressing the pro-adhesive phenotype of endothelial cells.