Modulation of the Uterine Response to Infectious Bacteria in Postpartum Ewes
Version of Record online: 7 MAR 2002
American Journal of Reproductive Immunology
Volume 47, Issue 1, pages 57–63, January 2002
How to Cite
SEALS, R. C. , WULSTER-RADCLIFFE, M. C. and LEWIS, G. S. (2002), Modulation of the Uterine Response to Infectious Bacteria in Postpartum Ewes. American Journal of Reproductive Immunology, 47: 57–63. doi: 10.1034/j.1600-0897.2002.1o062.x
- Issue online: 7 MAR 2002
- Version of Record online: 7 MAR 2002
- uterine infection
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 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 × 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 PGE2 treatment suppressed lymphocyte proliferation, regardless of PROG, and highlights a progesterone-independent level of regulation of uterine immune function.