title: Modulation of the uterine response to infectious bacteria in postpartum ewes.
abstract: OBJECTIVE
  Exogenous progesterone and prostaglandin E2 (PGE2) can downregulate uterine immune functions and render the uterus susceptible to bacterial infection.
  
  
  METHODS
  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.affiliation: Virginia Polytechnic Institute and State University, Blacksburg, USA.
authors.forename: Richard C
authors.initials: RC
authors.lastname: Seals
authors.forename: Meghan C
authors.initials: MC
authors.lastname: Wulster-Radcliffe
authors.forename: Gregory S
authors.initials: GS
authors.lastname: Lewis
mesh_terms: D000191:Actinomycetaceae; D000193:Actinomycetales Infections / Q000209:etiology / Q000276:immunology / Q000662:veterinary; D000818:Animals; D015232:Dinoprostone / Q000494:pharmacology; D004927:Escherichia coli Infections / Q000209:etiology / Q000276:immunology / Q000662:veterinary; D005260:Female; D066298:In Vitro Techniques; D008213:Lymphocyte Activation / Q000187:drug effects; D049590:Postpartum Period / Q000187:drug effects / Q000276:immunology; D011374:Progesterone / Q000494:pharmacology; D011645:Puerperal Infection / Q000209:etiology / Q000276:immunology / Q000662:veterinary*; D012756:Sheep; D012757:Sheep Diseases / Q000209:etiology* / Q000276:immunology; D014599:Uterus / Q000187:drug effects / Q000276:immunology
chemical_list: D011374:Progesterone; D015232:Dinoprostone