Postpartum uterine infections such as metritis, endometritis and mastitis have been considered as underlying causes for ovarian dysfunction in mammals. Almost all mammals, particularly dairy animals are susceptible to postpartum uterine infections, resulting in impaired fertility and economic loss. One of the factors for low fertility in females is ovarian dysfunction, which is exhibited as impaired growth and function of ovarian follicles by the postpartum infection. Immune system of mammals provides a host defence mechanism against pathogenic microbes through the recognition of pathogen-associated molecular patterns (PAMPs) and forming inflammasomes. Like immune cells, ovarian granulosa cells also exhibit a similar pattern of cytokine gene expressions on exposure to PAMPs. Genome-wide transcriptomic approaches explored the molecular mechanisms underlying the immune function of buffalo granulosa cells during endotoxin exposure. Understanding the molecular mechanism of ovarian dysfunction due to uterine infection would be helpful to implement various strategies to handle the adverse effects of postpartum uterine disease on fertility by developing potential therapeutics. Therefore, this article focuses on key factors that are responsible for postpartum infection and particularly summarizes the molecular mechanism of infection underlying the ovarian dysfunction in dairy animals.
Keywords: Endotoxin; granulosa cells; ovarian dysfunction; postpartum period; toll-like receptors; uterine infection.