17beta-estradiol suppresses TLR3-induced cytokine and chemokine production in endometrial epithelial cells |
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| Authors: | Margaret?J?Lesmeister Rebecca?L?Jorgenson Steven?L?Young Email author" target="_blank">Michael?L?MisfeldtEmail author |
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| Institution: | (1) Department of Molecular Microbiology and Immunology, University of Missouri-Columbia, School of Medicine, Columbia, MO, USA;(2) Department of Obstetrics and Gynecology, University of North Carolina Medical School, School of Medicine, Chapel Hill, NC, USA |
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| Abstract: | Background The human endometrium is an important site for contact between the host and pathogens ascending the reproductive tract, and
thus plays an important role in female reproductive tract immunity. Previous work in our laboratory has suggested that Toll-like
receptors (TLRs) are involved in endometrial epithelial recognition of pathogens and that ligation of endometrial TLRs results
in the production of cytokines and chemokines important for both immune and reproductive functions of the endometrium. We
have also demonstrated cyclic regulation of TLR3 mRNA and protein expression in human endometrium, suggesting that steroid
hormones might play a role in the expression and function of TLR3. In this study, the effects of 17beta-estradiol (E2) and
progesterone (P) on TLR3 expression and function in endometrial cell lines were investigated. |
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