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Chlamydia trachomatis is the most commonly diagnosed sexually transmitted infection in the UK, with over 200,000 positive diagnoses annually. The infection is thought to cause reproductive complications including problems in conceiving a pregnancy through to miscarriage and early or stillbirth. One potential reason Chlamydia may impact upon pregnancy is through disrupting the embryo implantation at the earliest stages of pregnancy is by altering the ability of specific cells that line the uterus called stromal cells to respond to the hormone progesterone, the hormone responsible for preparing the uterus for pregnancy. The results of this study showed that Chlamydial infection of these uterus lining stromal cells decreased the levels of specific progesterone sensitive markers which are associated with early embryo implantation, suggesting a loss of responsiveness to progesterone treatment. These changes were accompanied by a decrease in the levels of RNA for the progesterone receptor which is responsible for progesterone activity, suggesting that this is a potential mechanism through which Chlamydia could directly inhibit the effects of progesterone on uterine cells., Competing Interests: Nick Wheelhouse is an Associate Editor of Reproduction and Fertility. Nick Wheelhouse was not involved in the review or editorial process for this paper, on which he is listed as an author., (© 2021 The authors.)

Peritoneal surface epithelial (PSE) cells participate in adhesion formation following inflammatory injury yet adjacent ovarian SE (OSE) cells regenerate without scarification after ovulation. OSE cells show inflammation-associated expression of 11beta hydroxysteroid dehydrogenase type 1 (11betaHSD1) enzyme, enabling intracrine generation of anti-inflammatory cortisol to minimise tissue damage. We asked if human PSE cells show an 11betaHSD1 response to pro-/anti-inflammatory stimulation and if so, how the 11-oxoreductase activity generated compares with OSE. PSE collected from premenopausal women undergoing surgery for benign gynaecological conditions were used to establish primary PSE cell cultures that were treated for 48 h with interleukin-1alpha (IL-1alpha) with/without anti-inflammatory steroid (cortisol or progesterone). mRNA levels corresponding to the genes of interest (11betaHSD1, 11betaHSD2, cyclooxygenase-2, COX-2) were measured by quantitative RT-PCR. IL-1alpha (0.5 ng/ml) stimulated 11betaHSD1 and COX-2 mRNA levels in PSE cells but 11betaHSD2 was unaffected. Cortisol (1 microM), not progesterone (1 microM), increased 11betaHSD1 mRNA and synergistically enhanced IL-1alpha action. Cortisol suppressed IL-1alpha-stimulated COX-2 more effectively than progesterone. PSE cells had a significantly lower basal 11-oxoreductase enzyme activity than OSE cells; IL-1alpha did not significantly increase the 11-oxoreductase activity in PSE cells but did so in OSE cells. We conclude that PSE cells respond to IL-1alpha and anti-inflammatory steroids in qualitatively similar ways as OSE. However, the enzymatic activity of 11betaHSD1 is lower in PSE and less responsive to IL-1alpha. This could help explain why peritoneal healing often leads to adhesion formation, whereas postovulatory ovarian healing is scar-free.