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J Appl Physiol (April 13, 2006). doi:10.1152/japplphysiol.00166.2006
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Submitted on February 8, 2006
Accepted on March 16, 2006

Castration Prevents Suppression of MHC Class II (Ia) Expression on Macrophages Following Trauma-Hemorrhage

Stefan Mayr1, Christian Walz1, Peter Angele1, Thomas Hernandez-Richter1, Irshad H. Chaudry1, Florian Loehe1, Karl-Walter Jauch1, and Martin Kurt Angele1*

1 Department of Surgery, Klinikum Grosshadern, Ludwig-Maximilians University, Munich, Germany; Department of Trauma Surgery, University of Regensburg, Regensburg, Germany; Center for Surgical Research and Department of Surgery, University of Alabama at Birmingham, Birmingham, Alabama, United States

* To whom correspondence should be addressed. E-mail: martin.angele{at}med.uni-muenchen.de.

Several studies indicate that cell-mediated immune responses, i.e., macrophage (M{Phi}) cytokine release capacities, MHC class II (Ia) expression etc., are suppressed following trauma-hemorrhage in male mice. Testosterone has been shown to be responsible for the depression of macrophage cytokine responses in males following trauma-hemorrhage. Antigen presentation via MHC class II plays a key role in initiating and maintaining cell-mediated and humoral immune responses. It remains unknown, however, whether testosterone has any effect on MHC class II following trauma-hemorrhage. To study this, male C3H/HeN mice were castrated or sham-castrated 2 weeks prior to trauma (midline laparotomy) and hemorrhage (Hem) (blood pressure 35±5 mmHg for 90 min and resuscitation) or sham operation. Four hours thereafter, MHC class II (Ia) expression was measured using flow cytometry. The results indicate that MHC class II (Ia) expression on peritoneal and splenic M{Phi} was significantly suppressed in male mice following trauma-hemorrhage. Prior castration, however, prevented the depression in MHC class II (Ia) expression on peritoneal and splenic M{Phi} following trauma-hemorrhage. Castration did not affect MHC class II (Ia) expression in M{Phi} from sham mice. Thus, testosterone depresses MHC class II (Ia) expression on peritoneal and splenic M{Phi} following trauma-hemorrhage in males. Since MHC class II is necessary for an adequate immune response, our results suggest that depletion of male sex steroids or blockade of androgen receptors using agents such as flutamide might prevent immunosuppression via maintaining MHC class II (Ia) expression following trauma and severe blood loss.




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