The immune system plays an integral role in female fertility. Uterine inflammation due to infection or extrinsic stress have immediate and long-term implications for fertility. Common, acute postpartum uterine infections in cattle are associated with decreased fertility long after the resolution of disease. We hypothesize that uterine inflammation causes long-term alterations to tissues of the reproductive tract that compromise fertility after disease resolution. Using models of spontaneous uterine disease and induced uterine inflammation we have demonstrated long-term changes to the competence of uterine tissues to recognize and support early embryo development and facilitate pregnancy recognition. In parallel, granulosa cells of the developing ovarian follicle are exposed to pathogen components like lipopolysaccharide during uterine infections. Consequently, granulosa cells create an inflammatory environment in which oocytes develop. We have shown that oocytes collected from cows weeks after the occurrence of uterine inflammation have a decreased capacity to develop preimplantation stage embryos. Similarly, if oocytes are matured in an environment that mimics ovarian follicle inflammation, they too have a decreased capacity for further development. Granulosa cell inflammation also alters ovarian endocrine function. The capacity of granulosa cells to produce estradiol is diminished when exposed to pathogen components, and long-term steroidogenic capacity of subsequent luteal tissue is altered even after the resolution of disease. Collectively, we have demonstrated that inflammation of the female reproductive tract has both immediate and long-term implications for the capacity to generate and support future pregnancies long after the resolution of disease. While these discoveries are important in improving food security in animal agriculture, they also have implications for human fertility where sexually transmitted infections are common.