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Antiinflammatory Steroid Action in Human Ovarian Surface Epithelial Cells

Centre for Reproductive Biology, University of Edinburgh, Edinburgh EH16 4SB, United Kingdom

Address all correspondence and requests for reprints to: Michael T. Rae, Ph.D., Centre for Reproductive Biology, University of Edinburgh, Chancellors Building, 49 Little France Crescent, Edinburgh EH16 4SB, United Kingdom. E-mail: mrae1{at}staffmail.ed.ac.uk.

The human ovarian surface epithelium (OSE) is subject to serial injury and repair during ovulation, which is a natural inflammatory event. We asked whether there is a compensatory antiinflammatory component to this process, involving steroid hormones produced locally at the time of ovulation. Quantitative RT-PCR analysis of total RNA from cultured human OSE cell monolayers showed that exposure to proinflammatory IL1 (500 pg/ml) increased mRNA levels of cyclooxygenase-2 (COX-2) (P < 0.01) at 48 h. The COX-2 mRNA response to IL1 was associated with an approximate 18-fold (P < 0.01) increase in mRNA levels of 11ß-hydroxysteroid dehydrogenase type 1 (11ßHSD1), encoding the steroid dehydrogenase that reversibly reduces cortisone to antiinflammatory cortisol. Addition of cortisol to OSE cell culture medium dose-dependently suppressed the COX-2 mRNA response to IL1 (P < 0.01) but reciprocally enhanced the 11ßHSD1 mRNA response (P < 0.05), with both effects strongest at 1 µM cortisol. Presence of glucocorticoid receptor- mRNA and protein was established in OSE cell monolayers and treatment with IL1 shown to significantly up-regulate the glucocorticoid receptor- mRNA level (P < 0.05). Glucocorticoid receptor antagonist (RU486, 10 µM) fully reversed the inhibitory effect of 1 µM cortisol on IL1-stimulated COX-2 mRNA expression. Progesterone also suppressed IL1-induced COX-2 mRNA expression but had no significant effect on IL1-stimulated 11ßHSD1 expression. These data provide direct evidence for antiinflammatory actions of cortisol and progesterone in human OSE cells.

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