| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Articles in PresS, published online ahead of print February 6, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00560.2001
Submitted on November 20, 2001
Accepted on January 24, 2002
-dihydrotestosterone catabolism suppress T lymphocyte functions in males after trauma-hemorrhage
1 Surgery, University of Alabama School of Medicine, Birmingham, AL, USA
* To whom correspondence should be addressed. E-mail: irshad.chaudry{at}ccc.uab.edu.
Trauma-hemorrhage produces profound immunosuppression in males but not in proestrus females. Prior castration or Flutamide treatment of males following trauma-hemorrhage prevents immunosuppression, implicating 5-dihydrotestosterone for the immunosuppressive effects. 5-dihydrotestosterone, a high-affinity androgen receptor-binding steroid, is synthesized in tissues as needed and seldom accumulates. The presence of steroidogenic enzymes in T lymphocytes suggests both synthesis and catabolism of 5-dihydrotestosterone. We, therefore, hypothesized that the basis for high 5-dihydrotestosterone activity in T lymphocytes of males following trauma-hemorrhage is due to decreased catabolism. Accordingly, catabolism of 5-dihydrotestosterone was assessed in splenic T lymphocytes by examining the activity and expression of enzymes involved. Analysis showed increased synthesis and decreased catabolism of 5-dihydroteststerone in intact male T lymphocytes following trauma-hemorrhage. In contrast, reduced 5-reductase activity and increased expression of 17ß-hydroxysteroid dehydrogenase (17ß-HSD) oxidative isomers suggest inactivation of 5-dihydrotestosterone in pre-castrated males. Thus, our study establishes increased synthesis and decreased catabolism of 5-dihydrotestosterone as a reason for loss of T lymphocyte functions in intact males following trauma-hemorrhage, as evidenced by decreased release of IL-2 and IL-6.
This article has been cited by other articles:
|
|
 |
|
  T. Suzuki, T. Shimizu, H.-P. Yu, Y.-C. Hsieh, M. A. Choudhry, and I. H. Chaudry Salutary effects of 17beta-estradiol on T-cell signaling and cytokine production after trauma-hemorrhage are mediated primarily via estrogen receptor-{alpha} Am J Physiol Cell Physiol, June 1, 2007; 292(6): C2103 - C2111. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Mayr, C. R. Walz, P. Angele, T. Hernandez-Richter, I. H. Chaudry, F. Loehe, K. W. Jauch, and M. K. Angele Castration prevents suppression of MHC class II (Ia) expression on macrophages after trauma-hemorrhage J Appl Physiol, August 1, 2006; 101(2): 448 - 453. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Matsutani, T. S. A. Samy, L. W. Rue III, K. I. Bland, and I. H. Chaudry Transgenic prolactin-/- mice: effect of trauma-hemorrhage on splenocyte functions Am J Physiol Cell Physiol, May 1, 2005; 288(5): C1109 - C1116. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. M. Nitsch, F. Wittmann, P. Angele, M. W. Wichmann, R. Hatz, T. Hernandez-Richter, I. H. Chaudry, K. W. Jauch, and M. K. Angele Physiological Levels of 5{alpha}-Dihydrotestosterone Depress Wound Immune Function and Impair Wound Healing Following Trauma-Hemorrhage Arch Surg, February 1, 2004; 139(2): 157 - 163. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. S. A. Samy, R. Zheng, T. Matsutani, L. W. Rue III, K. I. Bland, and I. H. Chaudry Mechanism for normal splenic T lymphocyte functions in proestrus females after trauma: enhanced local synthesis of 17{beta}-estradiol Am J Physiol Cell Physiol, July 1, 2003; 285(1): C139 - C149. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
