dinoprost and Actinomycetales-Infections

To study ovarian responses to long-term intrauterine infusions of Trueperella pyogenes (T. pyogenes), 12 nonlacting Holstein cows were transcervically infused with 10 mL of a bacterial solution (8-19 × 10(8) colony-forming units/mL), and the uteri of another four cows (control) were similarly infused with sterile physiological saline. Infusions were done six times, every 3 days from Days 3 to 18 (Day 0 = day of spontaneous ovulation). Development of ovarian follicles and the CL were monitored with transrectal, real-time ultrasonography. In five of the experimentally infected cows (group A), the CL, which developed after Day 0, regressed without maturing, and the first dominant follicle (DF) ovulated (mean ± SEM interovulatory interval, 8.6 ± 0.5 days). In group A, plasma 13,14-dihydro-15-keto-PGF(2α) (PGFM) concentrations rose sharply on Day 6, but plasma progesterone concentrations did not increase substantially (as in the control) and were maintained at approximately 2.5 ng/mL after the first DF ovulated. In seven of the 12 infected cows (group B), the developing CL which formed after Day 0 matured and the second DF ovulated. However, the CL lifespan was shorter (P < 0.01) and the second DF ovulated earlier than in control (interovulatory interval, 16.0 ± 0.4 days and 22.3 ± 1.9 days; P < 0.01). Although there was no sharp increase in PGFM in group B, it tended to be high between Days 11 and 18. In conclusion, long-term, intrauterine infusions of T. pyogenes caused the CL to regress prematurely or to have a somewhat shorter lifespan because of release of endogenous PGF(2α).

Topics: Actinomycetaceae; Actinomycetales Infections; Animals; Cattle; Cattle Diseases; Corpus Luteum; Dinoprost; Estrous Cycle; Female; Ovulation; Progesterone; Ultrasonography; Uterine Diseases; Uterus

In sheep and cattle, the postpartum uterus is resistant to bacterial challenge until after corpora lutea develop. A 2 x 2 factorial arrangement of treatments was used 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 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 intramuscular injections of progesterone in sesame oil or plain sesame oil. On d 20, each uterus received 75 x 10(7) cfu of Arcanobacterium pyogenes and 35 x 10(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, prostaglandin F2alpha, (PGF2alpha), and prostaglandin E2 (PGE2) were quantified. All 12 progesterone-treated, but only two of the 12 oil-treated, ewes developed uterine infections (P < 0.001). 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) PGF2alpha, (303.9 vs 801.3 pg/mL), and PGF2alpha was greater (P < 0.05) before than after inoculation (626.4 vs 478.8 pg/mL). The PGE2 concentration was greater in progesterone-treated, ovary-intact ewes than in ewes in the other groups (ovariectomy x progesterone treatment; 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 x progesterone and progesterone x period interactions were significant (P < 0.01). The ovariectomy x progesterone 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 mechanism

Topics: Actinomycetales Infections; Animals; Dinoprost; Dinoprostone; Disease Susceptibility; Escherichia coli Infections; Female; Ovariectomy; Postpartum Period; Progesterone; Puerperal Infection; Random Allocation; Sheep; Sheep Diseases; Uterine Diseases; Uterus