When animals do not become pregnant, regression of the corpus luteum (CL) is essential for normal cyclicity because it allows the development of a new ovulatory follicle. Luteal regression is caused by a pulsatile release of prostaglandin (PG) F2α from the uterus in the late luteal phase in most mammals including cattle. Although it has been proposed in ruminants that pulsatile PGF2α secretion is generated by a positive feedback loop between luteal and/or hypophyseal oxytocin and uterine PGF 2α, the bovine endometrium may possess other mechanisms for initiation of luteolytic PGF2α secretion. There is increasing evidence that several cytokines mainly produced by immune cells modulate CL and uterine function in many species. Tumor necrosis factor-α (TNF-α) stimulates PGF2α output from bovine endometrium not only at the follicular phase but also at the late luteal phase. Administration of TNF-α at a high concentration prolongs luteal lifespan, whereas administration of a low concentration of TNF-α accelerates luteal regression in cows. The data obtained from the authors' previous in vitro and in vivo studies strongly suggest that TNF-α is a crucial factor in regulating luteolysis in cows. The authors' recent study has shown that interleukin-1α mediates PG secretion from bovine endometrium as a local regulator. Furthermore, interferon-τ (IFN-τ) suppresses the action of TNF-α on PGF2α synthesis by the bovine endometrium in vitro, suggesting that IFN-τ plays a luteoprotective role by inhibiting TNF-α-induced PGF2α production in early pregnancy. The purpose of the present review is to summarize current understanding of the endocrine mechanisms that regulate uterine function by cytokines during the estrous cycle and early pregnancy in cows.
- Tumor necrosis factor-α
ASJC Scopus subject areas
- General Agricultural and Biological Sciences