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Reproductive tract inflammatory disease (RTID) commonly occurs after the traumatic events of parturition and adversely affects follicular function. This study is the first to describe the cellular and steroidogenic characteristics of corpora lutea from cattle with RTID and the effects of pathogen-associated molecular patterns (PAMPs) on luteal angiogenesis and function  in vitro . Luteal weight ( P   3-fold lower in RTID cows ( P    0.05). Moreover, the adverse effect of LPS on luteal EC networks was dose-dependent and effective from 1 ng/mL ( P  &lt; 0.05), while few EC networks were present above 10 ng/mL LPS ( P  &lt; 0.001). LPS reduced proliferation ( P  &lt; 0.05) and increased apoptosis of EC ( P  &lt; 0.001). The specific TLR4 inhibitor TAK242 reversed the effects of LPS on EC networks. In conclusion, luteal vasculature is adversely sensitive to LPS acting via TLR4, therefore ovarian exposure to LPS from any Gram-negative bacterial infection will profoundly influence subsequent reproductive potential.

Detrimental effects of uterine disease and lipopolysaccharide on luteal angiogenesis