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This version published online on October 13, 2005
Endocrinology, doi:10.1210/en.2005-1113
A more recent version of this article appeared on January 1, 2006
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Submitted on August 31, 2005
Accepted on September 30, 2005

EXPRESSION AND FUNCTION OF TOLL-LIKE RECEPTOR 4 IN THE ENDOMETRIAL CELLS OF THE UTERUS

SHAN HERATH, DEBORAH P. FISCHER, DIRK WERLING, ERIN J. WILLIAMS, SONIA T. LILLY, HILARY DOBSON, CLARE E. BRYANT, and I. MARTIN SHELDON*

Royal Veterinary College, Department of Veterinary Clinical Sciences, University of London, Hawkshead Lane, North Mymms, Hatfield, Herts. AL9 7TA, UK; Royal Veterinary College, Department of Pathology and Infectious Diseases, University of London, Hawkshead Lane, North Mymms, Hatfield, Herts. AL9 7TA, UK; Department of Veterinary Clinical Science and Animal Husbandry, Faculty of Veterinary Science, University of Liverpool, Leahurst, Neston, CH64 7TE, UK; Centre for Veterinary Science, Department of Clinical Veterinary Medicine, University of Cambridge, Madingley Road, Cambridge, CB3 0ES, UK

* To whom correspondence should be addressed. E-mail: sheldon{at}rvc.ac.uk.

Prostaglandins have a central role in many endocrine functions in mammals, including regulation of the life span of the corpus luteum by prostaglandin F2{alpha} (PGF) and prostaglandin E2 (PGE), which are secreted by the uterine endometrium. However, the uterus is readily infected with bacteria such as Escherichia coli, which disrupt luteolysis. Immune cells detect Escherichia coli by toll-like receptor 4 (TLR4) binding its pathogenic ligand, lipopolysaccharide (LPS), although signaling requires accessory molecules such as CD14. The objective of this study was to determine the effect of Escherichia coli or LPS on the function of bovine endometrial cells, and whether purified populations of epithelial and stromal cells express the molecules involved in LPS recognition. In addition, as the female sex hormones estradiol and progesterone modify the risk of uterine infection, their effect on the LPS response was investigated. Endometrial explants produced prostaglandins in response to LPS, with an increased ratio of PGE to PGF. Addition of LPS or Escherichia coli to stromal and epithelial cells stimulated production of PGE and PGF, and increased their COX2 mRNA expression. The production of prostaglandins was abrogated by an LPS-antagonist. In addition, estradiol and progesterone inhibited the production of PGE and PGF in response to LPS, indicating a role for steroid hormones in the response to bacterial infection. For the first time, TLR4 mRNA and CD14 mRNA and protein were detected in bovine endometrial stromal and epithelial cells by RT-PCR and flow cytometry. In conclusion, epithelial and stromal cells detect and respond to bacteria, which modulate their endocrine function.
Key words: Inflammation • reproductive immunology • steroid influence




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