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Bacterial Lipopolysaccharide Induces an Endocrine Switch from Prostaglandin F₂ to Prostaglandin E₂ in Bovine Endometrium

Department of Veterinary Clinical Sciences (S.H., S.T.L., D.P.F., E.J.W.), Royal Veterinary College, London NW1 0TU, United Kingdom; Department of Veterinary Clinical Science and Animal Husbandry (H.D.), University of Liverpool, Neston CH64 7TE, United Kingdom; Department of Veterinary Medicine (C.E.B.), University of Cambridge, Cambridge CB3 0ES, United Kingdom; and Institute of Life Science (I.M.S.), School of Medicine, Swansea University, Swansea SA2 8PP, United Kingdom

Address all correspondence and requests for reprints to: Professor Martin Sheldon, Institute of Life Science, School of Medicine, Swansea University, Singleton Park, Swansea SA2 8PP, United Kingdom. E-mail: i.m.sheldon{at}swansea.ac.uk.

Escherichia coli infection of the endometrium causes uterine disease after parturition and is associated with prolonged luteal phases of the ovarian cycle in cattle. Termination of the luteal phase is initiated by prostaglandin F₂ (PGF) from oxytocin-stimulated endometrial epithelial cells. Compared with normal animals, the peripheral plasma of animals with E. coli infection of the endometrium had higher concentrations of lipopolysaccharide (LPS) and prostaglandin E₂ (PGE) but not PGF. Endometrial explants accumulated predominantly PGE in the culture medium in response to LPS, and this effect was not reversed by oxytocin. Endometrial cells expressed the Toll-like receptor 4/CD14/MD-2 receptor complex necessary to detect LPS. Epithelial and stromal cells treated with LPS had higher steady-state media concentrations of PGE rather than PGF. Arachadonic acid is liberated from cell membranes by phospholipase 2 (PLA2) enzymes and converted to prostaglandins by synthase enzymes. Treatment of epithelial and stromal cells with LPS did not change the levels of PGE or PGF synthase enzymes. However, LPS stimulated increased levels of PLA2 group VI but not PLA2 group IV C immunoreactive protein in epithelial cells. Endometrial cells expressed the E prostanoid 2 and E prostanoid 4 receptors necessary to respond to PGE, which regulates inflammation as well as being luteotropic. In conclusion, LPS detection by endometrial cells stimulated the accumulation of PGE rather than PGF, providing a mechanism to explain prolonged luteal phases in animals with uterine disease, and this PGE may also be important for regulating inflammatory responses in the endometrium.

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