Introduction: Ethanol (EtOH) intoxication plays an important role in the etiology of traumatic events and has often been described as having immunosuppressive effects. EtOH has been shown to affect intestinal barrier function in prior studies. The ability of gut derived factors on neutrophil function in this setting is unknown. This study looks at the role of ethanol in modulating proinflammatory states in the neutrophil in vitro.
Methods: Confluent Caco2 monolayers were exposed to 0.1% EtOH and/or Escherichia coli C-25 (EC) under normoxia (21% O(2)) or hypoxia (5% O(2)) followed by normoxic conditions (H/R). Neutrophils were then incubated with the supernatants from the treated cells. Chemotaxis, elastase and superoxide anion release, and CD11b measurements were undertaken in these neutrophils and compared with controls.
Results: In the presence of EtOH, Caco2 cells undergoing H/R and bacterial challenge demonstrated a proinflammatory effect on neutrophils. The production of both elastase and superoxide anion were significantly increased from controls. Additionally, the presence of EtOH in Caco2 cells undergoing H/R with/without EC showed a statistically significant increase in CD11b expression and chemotaxis, when compared with controls.
Conclusions: EtOH has a proinflammatory role in the activation of neutrophils at the intestinal epithelial cell barrier in shock states. EtOH may play an important role in worsening septic complication in severely traumatized patients via dysregulation of neutrophils.