Prostaglandin E2 promotes Staphylococcus aureus infection via EP4 receptor in bovine endometrium.

Prostaglandin E2 (PGE) enhances Staphylococcus aureus infection but its mechanism is not well understood. Here, we examined the effect of PGE on Staphylococcal Protein A (SPA) expression in bovine endometrium and determined the role of select PGE receptors (i.e., EP2 and EP4) in adhesion and internalization of S. aureus. S. aureus isolate SA113 was used for in vitro infection of bovine endometrial tissues and epithelial cells, with treatment conditions consisting of untreated control, SA113 treatment, SA113 + PGE, SA113 + PGE + EP2 receptor antagonist (AH-6809), and SA113 + PGE + EP4 receptor antagonist (AH-23848). Immunofluorescence assay revealed that PGE could promote SPA expression in S. aureus-infected bovine endometrial tissues. PGE also enhanced the adhesion and internalization of S. aureus in bovine endometrial cells. The addition of EP4 antagonist, but not the EP2 antagonist, abrogated the ability of PGE to promote S. aureus SPA expression, adhesion, and internalization in endometrial cells. Our findings suggest that S. aureus infection in the endometrium is enhanced by PGE through the EP4 receptor. This result is essential for the development of new approach to treating S. aureus infection, such as the application of EP4 antagonist as an adjunct drug treatment.