The impact of inflammatory genetics on oocyte viability and embryo development in women with chronic pelvic inflammatory disease

Infection by Chlamydia trachomatis is the leading cause of tubal disease and accounts for a significant proportion of the physical, psychosocial and economic burden of infertility. As it is frequently asymptomatic and opportunities for early treatment are missed, repeated/chronic infection leads to permanent/irreversible inflammation- induced tubal damage, which may extend as far as the ovary. However, not all infected women develop tubal pathology, possibly due to inherent host-specific and environment-induced differences in immune response. This study investigated the impact of putative cytokine-based gene and protein-mediated influences governing the host immune response to C. trachomatis infection and its effects on tubal pathology and ovarian function. The study population comprised 367 women whose infection status was determined serologically. Genetic predisposition to tubal disease was assessed by profiling single nucleotide polymorphism allelic variants in nine cytokines. Ovarian follicular fluid and circulatory cytokine profiles were determined by fluid-phase multiplex immunoassay, while serum antl-Mullerlan hormone levels were measured by enzyme-linked immunosorbent assay. No genetic or circulatory markers of susceptibility to tubal pathology were identified. Furthermore, tubal disease had no significant impact on ovarian function (based on ovarian reserve and follicular cytokine levels). The failure to identify genetic susceptibility markers of tubal disease may reflect the fact that the disease is under polygenic influence with superimposed environmental predisposing factors. Together with the fact that local inflammatory processes may not be reflected systemically, putative changes in cytokine profile between initial infection and the study period could explain why no serum biomarkers of tubal disease could be identified. Finally, the observation that tubal disease had no measurable effect on ovarian pathophysiology is likely to be due either to the small number of women with severe disease recruited to the study or due to other confounding factors eliminating the contribution of the infective inflammatory responses. Further investigation is thus warranted.