Abstract
Postpartum uterine infections reduce reproductive efficiency and have significant animal welfare and economic consequences. Postpartum uterine infections are classified as nonspecific, but Arcanobacterium pyogenes and Escherichia coli are usually associated with them in cattle and sheep. Pyometra is the most common type of uterine infection in dairy cattle, and it is detected almost exclusively in cows with active corpora lutea. Luteal progesterone typically down-regulates uterine immune functions and prevents the uterus from resisting infections. Progesterone also can down-regulate uterine eicosanoid synthesis. This seems to be a critical event in the onset of uterine infections, because eicosanoids can up-regulate immune cell functions in vitro. In addition, exogenous prostaglandin F2 alpha stimulates uterine secretion of prostaglandin F2 alpha and enhances immune functions in vivo. Thus, one may hypothesize that eicosanoids can override the negative effects of progesterone and that the up-regulatory effects of exogenous prostaglandin F2 alpha allow the uterus to resolve an infection, regardless of progesterone concentrations. Based on the results of studies to test that hypothesis, cows, sheep, and pigs in various physiological statuses are resistant to intrauterine infusions of Arcanobacterium pyogenes and Escherichia coli, unless progesterone concentrations are increased. In sheep and pigs, exogenous prostaglandin F2 alpha stimulates uterine production of prostaglandin F2 alpha and allows the uterus to resolve Arcanobacterium pyogenes-Escherichia coli-induced infections, even when progesterone is maintained at luteal phase concentrations before and after treatment. Prostaglandin F2 alpha is a proinflammatory molecule that stimulates the production of various proinflammatory cytokines, and it may enhance uterine production of leukotriene B4. Proinflammatory cytokines and leukotriene B4 enhance phagocytosis and lymphocyte functions. Even though there are clear associations among prostaglandin F2 alpha, leukotriene B4, proinflammatory cytokines, phagocytosis, and lymphocyte functions, the mechanism of action of exogenous prostaglandin F2 alpha in overriding the down-regulatory effects of progesterone and resolving uterine infections has not been elucidated. Defining this mechanism should yield new prevention and treatment strategies for uterine infections that do not rely on antibiotic and antimicrobial compounds.
Highlights
Nonspecific uterine infections reduce the reproductive efficiency of livestock [1,2,3]
They are called nonspecific because the initial colonizing bacterium is not known, and the specific bacteria causing the signs of infection are
In a variety of combinations, have been isolated from infected uteri, Arcanobacterium pyogenes and Escherichia coli are usually associated with uterine infections in cattle and sheep [3,4,5,6]
Summary
Nonspecific uterine infections reduce the reproductive efficiency of livestock [1,2,3]. Progesterone reduced unstimulated lymphocyte proliferation, whereas exogenous PGF2α increased unstimulated, Con A-stimulated, and LPS-stimulated lymphocyte proliferation The results of this experiment indicate that exogenous PGF2α enhances the ability of the uterus to resolve infections, regardless of progesterone concentrations. Concanavalin A, Con A; Interleukin, IL; Intramuscular, i.m.; Leukotriene B4, LTB4; Lipopolysaccharides, LPS; Phosphate-buffered saline, PBS; Phospholipase A2, PLA2; Prostaglandin F2α, PGF2α; 13,14-dihydro-15-keto-PGF2α, PGFM; Tumor-necrosis factor α, TNFα; If the assertion that enhancing uterine secretion of PGF2α and LTB4 will enable the uterus to resolve infections is correct, it means that PGF2α and LTB4 must override the inhibitory effects of progesterone. Even though progesterone has a variety of inhibitory effects, they are not always consistent among reports, much of the research has only been conducted with in vitro systems, and very little of the research has been focused on the relationship between production of various proinflammatory molecules and the ability of the uterus in livestock to resistant or resolve infections
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