Citation

Faunce DE, Gregory MS, Kovacs EJ. Shock 1998; 10(2): 135-140.

Affiliation

Department of Cell Biology, Neurobiology, and Anatomy, Loyola University Medical Center, Maywood, Illinois 60153, USA.

Copyright

(Copyright © 1998, The Shock Society, Publisher Lippincott Williams and Wilkins)

DOI

unavailable

PMID

9721981

Abstract

Previous studies by our laboratory have demonstrated that acute ethanol exposure prior to thermal injury results in suppression of cellular immune responses when compared with thermal injury alone. Ethanol exposure 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 ethanol (or vehicle) treatment. At 24 h post-injury, we observed slightly suppressed splenocyte proliferative responses and elevated circulating IL-6 (149+/-15 pg/mL) in mice receiving burn alone compared with those receiving sham injury (31+/-7 pg/mL). In contrast, burn + ethanol treated mice showed a profound suppression of splenocyte proliferation (20% of control) and significantly elevated circulating IL-6 levels (738+/-218 pg/mL). The suppressed splenocyte proliferative response was found to be macrophage dependent. Furthermore, IL-6 production was significantly elevated (p < .05) in splenic macrophage cultures from burn + ethanol mice (159+/-6 pg/mL) when compared with burn alone (109+/-10 pg/mL). Treatment of the splenocyte cultures from burn + ethanol mice with an anti-IL6 monoclonal antibody resulted in partial restoration of splenocyte proliferation. Taken together, these data strongly suggest that the immune dysfunction observed in ethanol-exposed, thermally injured mice is mediated in part by elevated levels of IL-6.

Language: en