Prostaglandins suppress neutrophil function after sexual intercourse and may promote urinary tract infections

• Women are at exceptionally high risk of developing urinary tract infections (UTIs). • Neutrophils play an important role in response to UTI-causing microbes. • Prostaglandins in seminal fluid exert control over neutrophil functions. • The interplay between seminal fluid and neutrophils provides insight into factors contributing to susceptibility to UTIs. Sexually active women have an increased risk of urinary tract infections (UTIs), which may be influenced by components in seminal plasma. Prostaglandins in seminal plasma are key modulators of the immune system and maternal-fetal immunological tolerance, influencing cells like platelets and neutrophils. Specifically, prostaglandin I2 (PGI2) inhibits platelet aggregation, while prostaglandin E2 (PGE2) alters neutrophil activity, including the production of reactive oxygen species (ROS) and the formation of neutrophil extracellular traps (NETs). Given that the NET response is associated with UTIs, and PGI2 is known to modulate NETs, these interactions may contribute to the higher incidence of UTIs in sexual activity in women. This study aims to investigate whether UTIs following sexual activity are facilitated by an imbalance in NET formation mediated by prostaglandins. We employed four search strategies: Sex and UTI, NETs and UTIs, Prostaglandins and NETs, and Inflammasome and NETs, alongside a review of original research publications. By understanding this mechanism, we hope to reveal how prostaglandin-mediated immune modulation may increase susceptibility to UTIs after sexual activity.