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Mechanisms linking infection and innate immunity in the female genital tract with infertility in dairy cattle
One of the most common endemic diseases of dairy cattle is bacterial infection of the uterus after parturition. These infections damage the endometrium lining the uterus, reduce the production of milk, and cause infertility. Uterine disease is caused by Escherichia coli, Trueperella pyogenes, anaerobic bacteria and viruses. These microbes posses a range of virulence factors that caused inflammation and damage in the endometrium. Innate immunity is an ancient system of defence against microbes, dependent on host cellular pattern recognition receptors such as Toll-like Receptors, which bind pathogen-associated molecular patterns. Epithelial and stromal cells are the first line of defence against microbes in the endometrium, and they express most Toll-like Receptors. Activation of Toll-like Receptor signalling leads to the secretion of chemokines, cytokines and prostaglandins, which attract and activate neutrophils and macrophages to clear the microbes. Microbial factors and host intracellular pathways regulate the scaling of the innate immune response, and the severity of postpartum uterine disease. Uterine disease also compromises ovarian function, with impacts on the corpus luteum, and on ovarian follicle development from primordial to antral follicles. Whilst healthy ovarian follicles are devoid of immune cells, granulosa cells express Toll-like Receptors and have roles in innate immunity. Pathogen-associated molecular patterns perturb granulosa cell endocrine function, stimulate the secretion of inflammatory mediators from granulosa cells, and lead to damage of oocytes. In conclusion, the fundamental mechanisms of innate immunity and inflammation in the female genital tract of dairy cattle are important for animal health and fertility.
Work in the Sheldon laboratory is funded by the Biotechnology and Biological Sciences Research Council (BBSRC) in the UK.
Keywords: dairy cattle, uterus, parturition