Effect Of Progesterone On Gonococci-Induced Apoptosis And Respiratory Burst Of Human Polymorphonuclear Leukocytes In Vitro

BackgroundProgesterone may have clinical relevance in females with asymptomatic gonococcal infections.AimTo investigate the regulatory effect of progesterone on apoptosis and oxidative burst activity of polymorphonuclear leukocytes (PMNs) challenged by Neisseria gonorrhoeae in vitro.MethodsIsolated PMNs were incubated with progesterone or staurosporine. Staurosporine was used as a positive control for our in vitro model. Expression levels of inhibitory apoptosis proteins (IAPs), cellular IAP2 (cIAP2), and X-linked IAP (XIAP) were determined by real-time polymerase chain reaction (PCR). In addition, PMN apoptosis at various time points (3, 8, 12, and 24 h) was assayed by flow cytometry. Luminol amplified chemiluminescence methods were used to quantify the oxidative burst function of PMNs challenged with N. gonorrhoeae ST2951.ResultscIAP2 was upregulated significantly in PMNs with progesterone treatment in 3 h, and XIAP was upregulated slightly compared with the medium + ST2951 group, whereas cIAP2 was downregulated in staurosporine-challenged PMNs. In addition, we found that progesterone delayed the onset of apoptosis activity in N. gonorrhoeae ST2951-challenged PMNs, notably at 12 h. No statistically significant changes in PMN oxidative burst activity were observed at 10 ng/mL of progesterone. Staurosporine enhanced the production of superoxide anion (respiratory burst) of human PMNs stimulated by N. gonorrhoeae.ConclusionProgesterone plays an important regulatory role in the interaction of PMNs and N. gonorrhoeae. Delayed PMN apoptosis induced by progesterone presumably acts as a mechanism for N. gonorrhoeae to avoid the innate immune response and establish long-term, low-level infection in the female reproductive tract.