• Parth B Amin, Lawrence N Diebel, and David M Liberati.
• Department of Surgery, Wayne State University/University Health Center 6-C, Detroit, Michigan, USA. pamin@dmc.org
• J Trauma. 2007 Dec 1;63(6):1223-9.

BackgroundEthanol (EtOH) intoxication increases posttraumatic infectious complications. EtOH is thought to be immunosuppressive, but the effect of the interaction with the gut and associated microflora on host defense is unknown. We studied the ability of intestinal epithelial cells and bacteria to modulate EtOH effects on polymorphonuclear (PMN) cell function in vitro.MethodsConfluent Caco2 monolayers were exposed to 0.1% EtOH with or without Escherichia coli on the apical side of each chamber. Supernatants were collected from the basal side of the chambers and incubated with neutrophils. Controls were incubated with or without 0.1% EtOH alone. Chemotaxis, elastase, and superoxide anion release, and CD11b measurements were undertaken in these neutrophils and compared with controls.ResultsAlcohol exhibited differing effects on the inflammatory potential of neutrophils in regards to CD11b expression, elastase production, and superoxide production. Direct effects of EtOH were anti-inflammatory, whereas indirect effects of EtOH on neutrophils modulated by Caco2 cells were proinflammatory. Chemotaxis was significantly reduced when neutrophils were directly treated with alcohol.ConclusionEtOH direct downregulates PMN inflammatory potential, but its impact of the intestinal epithelial cells produces a proinflammatory microenvironment for PMNs. The interaction of EtOH on the intestinal milieu may lead to neutrophil activation and increased organ injury after trauma in the intoxicated patient.

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