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J Appl Physiol (October 5, 2006). doi:10.1152/japplphysiol.00964.2006
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Submitted on August 31, 2006
Accepted on October 1, 2006

TISSUE-COMPARTMENT-SPECIFIC ROLE OF ESTROGEN RECEPTOR SUBTYPES IN IMMUNE CELL CYTOKINE PRODUCTION FOLLOWING TRAUMA-HEMORRHAGE

Takao Suzuki1, Tomoharu Shimizu1, Huang-Ping Yu2, Ya-Ching Hsieh1, Mashkoor A Choudhry1, Martin G. Schwacha3, and Irshad H. Chaudry4*

1 Surgery, University of Alabama at Birmingham, Birmingham, Alabama, United States
2 Anesthesiology, Chang Gung University, Taoyuan, Taiwan - Republic of China
3 Center for Surgical Research, U Alabama at Birmingham, Birmingham, Alabama, United States; Surgery, University of Alabama at Birmingham, Birmingham, Alabama, United States
4 Center for Surgical Research, U Alabama at Birmingham, Birmingham, Alabama, United States; , Alabama, United States

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

Although 17{beta}-estradiol administration following trauma-hemorrhage attenuates plasma cytokines and alteration in immune cell cytokine production, it is not known whether the salutary effects are mediated via estrogen receptor (ER)-{alpha} or ER-{beta}. Accordingly, we examined which ER subtype predominantly mediates the salutary effects of 17{beta}-estradiol on systemic inflammatory response/immune cell cytokine production in various tissues following trauma-hemorrhage. Male rats underwent trauma-hemorrhage (mean BP 40 mmHg for 90 min) and fluid resuscitation. The ER-{alpha} agonist propyl pyrazole triol (PPT) (5 µg/kg), the ER-{beta}- agonist diarylpropionitrile (DPN) (5 µg/kg), E2 (50 µg/kg) or vehicle (10% DMSO) was injected subcutaneously during resuscitation and various measurements were made 24 h thereafter. 17{beta}-estradiol or PPT administration following trauma-hemorrhage prevented the increase in plasma IL-6 and IL-10 levels that were observed in vehicle-treated animals. IL-6 and TNF-{alpha} production by Kupffer cells increased, however, splenic macrophages (SM{Phi}), alveolar macrophages (AM{Phi}) and peripheral blood mononuclear cells (PBMC) had decreased release of these cytokines after trauma-hemorrhage. IL-10 production, however, increased in all M{Phi} populations. Administration of 17{beta}-estradiol following trauma-hemorrhage prevented all of these alterations. PPT had the same effects as E2 on IL-6 and TNF-{alpha} production by Kupffer cells and SM{Phi}, and DPN had the same effects on AM{Phi} and PBMC. The same effects as 17{beta}-estradiol on IL10 production were observed by PPT on Kupffer cells and DPN on PBMC. Both agonists were equally effective on SM{Phi} and AM{Phi}. Thus, ER subtypes have tissue compartment-specific roles in mediating the effects of 17{beta}-estradiol on immune cell functions following trauma-hemorrhage.




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