PROBLEM: Exogenous progesterone and prostaglandin E2 (PGE2) can downregulate uterine immune functions and render the uterus susceptible to bacterial infection. METHOD OF STUDY: Ewes were sham-ovariectomized (SHAM) or ovariectomized (OVEX) 9 days after parturition (day 0), and their uteri were inoculated with Arcanobacterium pyogenes and Escherichia coli on day 15. Vena caval blood was collected on day 14 and days 16-19, and uteri were collected on day 20. Ewes began receiving either canola oil (OIL) or progesterone in oil (PROG) on day 10. Lymphocytes from each blood sample were assigned to a 2 x 2 factorial array of in vitro treatments; 10(-7) M PGE2 and 10(-7) M indomethacin (INDO) were main effects. [3H]Thymidine incorporation (expressed in picomoles) was used to quantify proliferation. RESULTS: Progesterone was greater (P = 0.001) in PROG than in OIL ewes (3.6 versus 0.7 ng/mL), and only PROG ewes developed infections. Lymphocyte proliferation was least (P = 0.02) in PROG-OVEX ewes (4.1 versus 5.4, 5.7, and 5.8 pmol for OIL-SHAM, PROG-SHAM, and OIL-OVEX, respectively). Concanavalin A (Con-A)-stimulated proliferation was less (P < 0.01) for PGE2- and PGE2 + INDO-treated lymphocytes (7.5 and 8.3 pmol, respectively) than for control or INDO-treated cells (12.9 and 14.7 pmol, respectively). CONCLUSIONS: Progesterone treatment of postpartum ewes suppressed uterine immunity. In vitro PGE, treatment suppressed lymphocyte proliferation, regardless of PROG, and highlights a progesterone-independent level of regulation of uterine immune function.
PROBLEM: Exogenous progesterone and prostaglandin E2 (PGE2) can downregulate uterine immune functions and render the uterus susceptible to bacterial infection. METHOD OF STUDY: Ewes were sham-ovariectomized (SHAM) or ovariectomized (OVEX) 9 days after parturition (day 0), and their uteri were inoculated with Arcanobacterium pyogenes and Escherichia coli on day 15. Vena caval blood was collected on day 14 and days 16-19, and uteri were collected on day 20. Ewes began receiving either canola oil (OIL) or progesterone in oil (PROG) on day 10. Lymphocytes from each blood sample were assigned to a 2 x 2 factorial array of in vitro treatments; 10(-7) M PGE2 and 10(-7) M indomethacin (INDO) were main effects. [3H]Thymidine incorporation (expressed in picomoles) was used to quantify proliferation. RESULTS:Progesterone was greater (P = 0.001) in PROG than in OIL ewes (3.6 versus 0.7 ng/mL), and only PROG ewes developed infections. Lymphocyte proliferation was least (P = 0.02) in PROG-OVEX ewes (4.1 versus 5.4, 5.7, and 5.8 pmol for OIL-SHAM, PROG-SHAM, and OIL-OVEX, respectively). Concanavalin A (Con-A)-stimulated proliferation was less (P < 0.01) for PGE2- and PGE2 + INDO-treated lymphocytes (7.5 and 8.3 pmol, respectively) than for control or INDO-treated cells (12.9 and 14.7 pmol, respectively). CONCLUSIONS:Progesterone treatment of postpartum ewes suppressed uterine immunity. In vitro PGE, treatment suppressed lymphocyte proliferation, regardless of PROG, and highlights a progesterone-independent level of regulation of uterine immune function.
Authors: Rachel L Piersanti; Roney Zimpel; Paula C C Molinari; Mackenzie J Dickson; Zhengxin Ma; KwangCheol C Jeong; José E P Santos; I Martin Sheldon; John J Bromfield Journal: J Dairy Sci Date: 2019-01-26 Impact factor: 4.034