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Am J Physiol Cell Physiol (March 26, 2003). doi:10.1152/ajpcell.00058.2003
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Submitted on February 11, 2003
Accepted on March 17, 2003

Mechanism for the maintenance of splenic T lymphocyte functions in proestrus females following trauma-hemorrhage: Enhanced local synthesis of 17{beta}-estradiol

T. S. Anantha Samy1, Rui Zheng1, Takeshi Matsutani1, Loring W. Rue1, Kirby I. Bland1, and Irshad H. Chaudry1*

1 Department of Surgery, University of Alabama at Birmingham, Birmingham, AL, USA

* To whom correspondence should be addressed. E-mail: Irshad.Chaudry{at}ccc.uab.edu.

Trauma-hemorrhage and resuscitation (TH) produces profound immunodepression and enhances susceptibility to sepsis in males but not in proestrus females, suggesting gender dimorphism in the immune responses. However, the mechanism responsible for the maintenance of immune functions in proestrus females following TH is unclear. Splenic T lymphocytes express receptors for estrogen (ER), contain enzymes involved in estrogen metabolism and are the major source of cytokine production; the metabolism of 17{beta}-estradiol was assessed in the splenic T lymphocytes of proestrus and ovariectomized mice by using appropriate substrates following TH. Analysis for aromatase and 17{beta}-hydroxysteroid dehydrogenases indicated increased 17{beta}-estradiol synthesis and low conversion into estrone in T lymphocytes of proestrus but not of ovariectomized mice. The effect of 17{beta}-estradiol on T lymphocyte cytokine release was reliant upon ER expressions. This was apparent in the differences of ER expression, especially that of ER-{beta}, and an association between increased 17{beta}-estradiol synthesis and sustained release of IL-2 and IL-6 in T lymphocytes of proestrus females following TH. Since 17{beta}-estradiol is able to regulate cytokine genes and the splenic T lymphocyte cytokine releases is altered following TH, continued synthesis of 17{beta}-estradiol in proestrus females appears to be responsible for the maintenance of T lymphocyte cytokine release associated with the protection of immune functions following TH.




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