ACUTE ETHANOL EXPOSURE PRIOR TO THERMAL-INJURY RESULTS IN DECREASED T-CELL RESPONSES MEDIATED IN PART BY INCREASED PRODUCTION OF IL-6

Previous studies by our laboratory have demonstrated that acute ethano l exposure prior to thermal injury results in suppression of cellular immune responses when compared with thermal injury alone. Ethanol expo sure and burn injury are independently known to result in elevated IL- 6, a cytokine with potent immunosuppressive properties. Therefore, we examined the role of IL-6 in the immune dysfunction in mice following a 15% body surface area scald (or sham) injury combined with acute eth anol (or vehicle) treatment. At 24 h post-injury, we observed slightly suppressed splenocyte proliferative responses and elevated circulatin g IL-6 (149 +/- 15 pg/mL) in mice receiving burn alone compared with t hose receiving sham injury (31 +/- 7 pg/mL). In contrast, burn + ethan ol treated mice showed a profound suppression of splenocyte proliferat ion (20% of control) and significantly elevated circulating IL-6 level s (738 +/- 218 pg/mL), The suppressed splenocyte proliferative respons e was found to be macrophage dependent. Furthermore, IL-6 production w as significantly elevated (p < .05) in splenic macrophage cultures fro m burn + ethanol mice (159 +/- 6 pg/mL) when compared with burn alone (109 +/- 10 pg/mL). Treatment of the splenocyte cultures from burn + e thanol ice with an anti-IL6 monoclonal antibody resulted in partial re storation of splenocyte proliferation. Taken together. these data stro ngly suggest that the immune dysfunction observed in ethanol-exposed, thermally injured mice is mediated in part by elevated levels of IL-6.