Modulation of the Uterine Response to Infectious Bacteria in Postpartum Ewes

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Abstract
PROBLEM: Exogenous progesterone and prostaglandin E2(PGE2) can down‐regulate 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 withArcanobacterium pyogenesandEscherichia colion 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 × 2 factorial array ofin vitrotreatments; 10–7 M PGE2and 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 vitroPGE2treatment suppressed lymphocyte proliferation, regardless of PROG, and highlights a progesterone‐independent level of regulation of uterine immune function.