Bacterial infection is widely recognised as a factor contributing to adverse pregnancy outcomes (APOs). Neisseria gonorrhoeae infections continue to be a universal and intractable problem. In this regard, maternal gonorrhoea increases a woman’s risk for APO by 6.5-fold. Bacterial infection is thought to trigger a pro-inflammatory response that initiates those processes involved in (preterm) human parturition. The ability of gonococci to invade and transcytose amniotic sac tissues, in vivo, is inferred from the ability to isolate gonococci from these tissues and from amniotic fluid. However, there are currently no data to indicate how gonococcal infection can result in APO, and a physiologically relevant human model of pregnancy that is amendable to scientific analyses has hindered elucidation of factors contributing to APO. Thereby, an understanding of gonococcal infection as it relates to human pregnancy, using human cell models of disease, could provide new insights into the pathophysiology of gonococcal disease and of APO as they likely occur in vivo. To this end, we investigated gonococcal infection under conditions reflecting normal pregnancy by using primary epithelial cells derived from the human cervix (i. e. pex cells) and amniochorionic membranes (i. e. pace cells) and by altering the combined concentrations of pertinent steroid hormones. Comparative, quantitative, infection assays indicated that gonococci adhere to and invade amniochorionic cells and tissue, which was further observed to occur by a complement receptor-mediated mechanism. We demonstrate that N. gonorrhoeae infection of pex and pace cells elicits the differential production of nitric oxide and complement proteins, as well as the specific matrix metalloproteases, prostaglandins, and cytokines thought to participate in triggering the onset of human parturition. Hence, we provide the first direct evidence to indicate a potential link between gonococcal infection and the induction of APOs.