Inflammatory Response in Multiple Organs in a Mouse Model of Acute Alcohol Intoxication and Burn Injury

This study characterized the inflammatory response after burn injury and determined whether ethanol (EtOH) intoxication at the time of burn injury influences this response. To accomplish this, male mice were gavaged with EtOH (2.9 g/kg) 4 hours before 12 to 15% TBSA sham or burn injury. Mice were killed on day 1 after injury; blood, small intestine, lung, and liver were collected to measure interleukin (IL)-6, IL-10, IL-18, and Monocyte chemotactic protein-1 (MCP-1) levels. In addition, neutrophil infiltration, myeloperoxidase activity, and edema formation were also measured in the small intestine, lung, and liver. There was no difference in the inflammatory markers in the small intestine, lung, and liver in mice receiving either sham or burn injury alone except IL-6 that was increased in all four tissue compartments after burn injury alone. However, when compared with EtOH or burn injury alone, EtOH combined with burn injury resulted in a significant increase in cytokines, neutrophil infiltration, myeloperoxidase activity, and edema in the small intestine, liver, and lung tissue. Furthermore, a significant increase in IL-6 and MCP-1 was observed in circulation after EtOH intoxication and burn injury compared with either EtOH intoxication or burn injury alone; no other cytokines were detected in circulation. These findings suggest that acute EtOH intoxication exacerbates the inflammatory response after burn injury. (J Burn Care Res 2011;32:489-497)