Submitted to: Journal of Animal Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: September 21, 2002
Publication Date: January 9, 2003
Citation: Lewis, G.S. Role of the ovaries and exogenous progesterone and potential role of prostaglandin F2A and prostaglandin E2 in modulating the uterine response to infestious bacteria in postpartum ewes. Journal of Animal Science. 2003. v. 81. p. 285-293 Interpretive Summary: Nonspecific uterine infections and their adverse effects on uterine health can reduce reproductive efficiency of ruminant livestock. This is well documented for dairy cattle, but very poorly documented for beef cattle and sheep. Postpartum ewes are exposed to many of the same risk factors that predispose dairy cattle to uterine infections. This research indicates that, under the appropriate hormonal conditions, postpartum ewes become susceptible to infectious bacteria and develop purulent uterine infections. The research also indicates that a method for enhancing uterine production of PGF2a may enhance immune functions and enhance the ability of the uterus to resist infections. A method for enhancing uterine health may improve reproductive efficiency.
Technical Abstract: In sheep and cattle, the postpartum uterus is resistant to bacterial challenge until after functional corpora lutea develop. This study was conducted to determine whether prostaglandins may mediate the effects of progesterone in transforming the postpartum uterus from resistant to susceptible. On d 14 postpartum, ewes (n = 6/group) were either ovariectomized or sham ovariectomized, and the vena cava was catheterized for daily collection of uteroovarian-enriched blood. From d 15 to 20, ewes received twice daily i.m. injections of either progesterone in sesame oil or sesame oil. On d 20, each uterus received 75 x 10(E 7) cfu of Arcanobacterium pyogenes and 35 x 10(E 7) cfu of Escherichia coli. Uteri were collected on d 25 and examined for signs of infection. For each blood sample, unstimulated and mitogen-stimulated lymphocyte proliferation was measured as [3H]thymidine incorporation, smears were prepared for differential white blood cell (WBC) counts, and progesterone, PGF2a, and PGE2 were quantified. All 12 progesterone-treated, but only 2 of 12 oil-treated, ewes developed uterine infections. Progesterone treatment increased (P < 0.001; 3.1 vs 1.5 ng/mL) and ovariectomy decreased (P < 0.001; 3.7 vs 0.9 ng/mL) vena caval progesterone. Progesterone treatment reduced (P < 0.01) PGF2a (303.9 vs 801.3 pg/mL), and PGF2a was greater (P < 0.05) before than after inoculation (626.4 vs 478.8 pg/mL). For PGE2, the ovariectomy ´ progesterone-treatment interaction was significant (P < 0.01). Ovariectomy increased (P < 0.005; 4.4 vs 2.9 pmol) and progesterone treatment decreased (P < 0.05; 3.2 vs 4.1 pmol) concanavalin A-stimulated lymphocyte proliferation. Ovariectomy increased lipopolysaccharides-stimulated proliferation (P < 0.05; 2.4 vs 1.9 pmol). For neutrophils per 100 WBC, the ovariectomy ´ progesterone-treatment and progesterone-treatment ´ period interactions were significant (P < 0.01). The ovariectomy ´ progesterone-treatment interaction was significant (P < 0.01) for lymphocytes per 100 WBC. Ovariectomy decreased monocytes (P < 0.001; 10 vs 13) and increased eosinophils (P < 0.001; 10 vs 5) per 100 WBC. Progesterone makes the postpartum uterus in ewes susceptible to infection, but ovariectomy allows ewes to remain resistant; uterine prostaglandins may mediate this change. This model creates opportunities to determine the mechanisms responsible for the shift from resistance to susceptible.