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1 Department of Trauma-Surgery, University of Ulm, Ulm, Germany
2 Department of Surgery, Klinikum Grosshadern, Munich, Germany
3 Center for Surgical Research and Department of Surgery, Brown University School of Medicine and Rhode Island Hospital, Providence, RI, USA
4 Center for Surgical Research and Department of Trauma-Surgery, University of Alabama at Birmingham, Birmingham, AL, USA
5 Center for Surgical Research and Department of Trauma-Surgery, University of Alabama at Birmingham, Birmingham, AL, USA; Department of Surgery, Klinikum Grosshadern, Munich, Germany
* To whom correspondence should be addressed. E-mail: Irshad.Chaudry{at}ccc.uab.edu.
Studies indicate that administration of the adrenal steroid dehydroepiandrosterone (DHEA) following trauma-hemorrhage in male mice improved cellular immune functions and reduced mortality rates from subsequent sepsis. There is evidence, however, that DEHA is converted to estrogens in males and that estrogens are immunoprotective following trauma-hemorrhage. In contrast, DHEA in females can be converted to testosterone that has deleterious effects on immune functions. The aim of our study therefore was to determine whether administration of DHEA in proestrus females following trauma-hemorrhage (T-H) would deteriorate immune responses. Proestrus female C3H/HeN mice (age 7-8 wk) were subjected to laparotomy (i.e., soft tissue trauma induced) and hemorrhagic shock (35±mmHg for 90 min) or sham operation. The mice then received DHEA (100 µg/25 g BW) or vehicle s.c. followed by fluid resuscitation (4 X the shed blood volume). Plasma IL-6, splenocyte proliferation, splenocyte IL-2, IL-3, IFN-
, IL-10 release and splenic M
IL-1
, IL-6, IL-10 and IL-12 release were determined 24 hr after T-H. Plasma IL-6 levels were significantly increased in vehicle treated females and DHEA administration markedly attenuated this response. In vehicle treated females, splenocyte proliferation, IL-2, IL-3 and IFN- release and splenic M IL-1, IL-6 and IL-12 release was maintained or slightly enhanced following T-H. In DHEA treated females, however, these immune functional parameters were either unaltered compared to vehicle treated animals or even further enhanced, but surprisingly not depressed. Moreover, DHEA reduced splenocyte and splenic M anti-inflammatory cytokine (i.e., IL-10) production following T-H compared with vehicle treated females. Since DHEA further enhances the immune responsiveness in proestrus females following T-H, this hormone might be a useful adjunct even in females for further enhancing immune responses and decreasing the mortality rate following trauma and severe blood loss.
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