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1 Center for Surgical Research and Department of Surgery, University of Alabama at Birmingham, Birmingham, AL, USA
2 Alcohol Research Program, Loyola University Chicago Medical Center, Maywood, IL, USA; Cell Biology Neurobiology and Anatomy, Loyola University Chicago Medical Center, Maywood, IL, USA
3 Alcohol Research Program, Loyola University Chicago Medical Center, Maywood, IL, USA; Surgery, Loyola University Chicago Medical Center, Maywood, IL, USA
* To whom correspondence should be addressed. E-mail: mashkoor.choudhry{at}ccc.uab.edu.
Our previous studies showed that alcohol (EtOH) intoxication prior to burn injury suppresses mesenteric lymph nodes (MLN) T cell functions and increases gut bacterial translocation. In this study, we examined whether corticosterone (CORT) plays any role in suppressing MLN T cell function and bacterial accumulation following EtOH intoxication and burn injury. Rats were gavaged with EtOH to achieve a blood EtOH level in the range of ~100 mg/dL prior to receiving 25% total body surface area burn or sham injury. A group of rats was treated with CORT synthesis inhibitor metyrapone (25 mg/kg) at the time of injury and on day one after injury. Two days after injury, a significant increase in blood CORT levels and suppression in MLN T cell proliferation and IL-2 production was observed in rats receiving a combined insult of EtOH intoxication and burn injury as compared to rats receiving either EtOH intoxication or burn injury alone. There was no change in T cell apoptosis following a combined insult of EtOH and burn injury. Furthermore, T cell suppression was accompanied by a significant decrease in p-38 and ERK-1/2 activation (i.e., phosphorylation). There was no difference in JNK activation following EtOH and burn injury. Treatment of rats with CORT synthesis inhibitor metyrapone prevented the suppression in MLN T cell proliferation, IL-2 production, and p-38 and ERK-1/2 phosphorylation. The restoration of T cell function in metyrapone-treated animals was also associated with the decrease in bacterial accumulation in MLN. These findings suggest that EtOH intoxication prior to burn injury augments CORT release which in turn suppresses MLN T cell function by inhibiting p-38 and ERK-1/2 activation, and promotes bacterial accumulation in MLN following EtOH and burn injury.
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