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Acute alcohol intoxication increases interleukin-18-mediated neutrophil infiltration and lung inflammation following burn injury in rats

¹Center for Surgical Research and Department of Surgery, University of Alabama at Birmingham, Birmingham, Alabama; and ²Alcohol Research Program, Burn and Shock Trauma Institute, Departments of Surgery and Cell Biology, Neurobiology, and Anatomy, Loyola University Chicago Medical Center, Maywood, Illinois

Submitted 16 October 2006 ; accepted in final form 11 January 2007

In this study, we examined whether IL-18 plays a role in lung inflammation following alcohol (EtOH) and burn injury. Male rats (250 g) were gavaged with EtOH to achieve a blood EtOH level of 100 mg/dl before burn or sham injury (12.5% total body surface area). Immediately after injury, rats were treated with vehicle, caspase-1 inhibitor AC-YVAD-CHO to block IL-18 production or with IL-18 neutralizing anti-IL-18 antibodies. In another group, rats were treated with anti-neutrophil antiserum 16 h before injury to deplete neutrophils. On day 1 after injury, lung tissue IL-18, neutrophil chemokines (CINC-1/CINC-3), ICAM-1, neutrophil infiltration, MPO activity, and water content (i.e., edema) were significantly increased in rats receiving a combined insult of EtOH and burn injury compared with rats receiving either EtOH intoxication or burn injury alone. Treatment of rats with caspase-1 inhibitor prevented the increase in lung tissue IL-18, CINC-1, CINC-3, ICAM-1, MPO activity, and edema following EtOH and burn injury. The increase in lung IL-18, MPO, and edema was also prevented in rats treated with anti-IL-18 antibodies. Furthermore, administration of anti-neutrophil antiserum also attenuated the increase in lung MPO activity and edema, but did not prevent the increase in IL-18 levels following EtOH and burn injury. These findings suggest that acute EtOH intoxication before burn injury upregulates IL-18, which in turn contributes to increased neutrophil infiltration. Furthermore, the presence of neutrophils appears to be critical for IL-18-meditaed increased lung tissue edema following a combined insult of EtOH and burn injury.

inflammatory mediators; adhesion molecule; chemokines

This article has been cited by other articles:

				M. D. Bird and E. J. Kovacs Organ-specific inflammation following acute ethanol and burn injury J. Leukoc. Biol., September 1, 2008; 84(3): 607 - 613. [Abstract] [Full Text] [PDF]