TOWNSON, D.H.; University of New Hampshire: Immune cell-endothelial cell interactions in the bovine corpus luteum.

Early embryonic mortality accounts for a substantial portion of reproductive failure in agriculturally important livestock, including the dairy cow. The maintenance of early pregnancy requires a fully functional corpus luteum that is not susceptible to regression following fertilization, yet the cellular mechanisms of luteal regression are not clearly understood. Immune cell accumulation within the corpus luteum at the time of luteal regression is a well-documented phenomenon in a variety of species. In the dairy cow, immune cell accumulation precedes luteal regression by several days and coincides with an increase in the expression of monocyte chemoattractant protein-1 (CCL2), suggesting that immune-mediated events promote the onset of tissue destruction. Our laboratory has shown that endothelial cells comprising the corpus luteum are a primary source of CCL2 secretion. Moreover, we know that although uterine-derived prostaglandin F2-alpha (PGF) initiates luteal regression in the cow, PGF does not directly provoke CCL2 secretion by luteal endothelial cells. Instead, it is proposed that PGF-induced luteal regression requires the cooperative interaction among immune cells, endothelial cells, and the steroidogenic cells within the corpus luteum to promote CCL2 secretion, enhance immune cell recruitment, and eliminate luteal tissue. This presentation will focus on proposed interactions between immune cells and endothelial cells derived from the bovine corpus luteum that result in enhanced CCL2 expression and the elaboration of other inflammatory mediators (e.g., cytokines, endothelin-1) that perpetuate luteal regression. Our long-term goal is to obtain fundamental knowledge of immune-endocrine interactions regulating the function of the corpus luteum and thereby formulate methods to improve estrous synchronization and fertility in cattle.