Progesterone increases susceptibility of gilts to uterine infections after intrauterine inoculation with infectious bacteria.

In cattle and sheep, a progestogenated uterus is susceptible to infections, but this is not well documented for pigs. Therefore, the effects of day of the estrous cycle and progesterone on the susceptibility to uterine infections were evaluated. Gilts (n = 5 per group) were assigned to treatments in 2 x 2 factorial arrays. In Exp. 1, day of cycle and bacterial challenge were main effects. On d 0 or 8, uteri were inoculated with either 70 x 10(7) cfu of Escherichia coli and 150 x 10(7) cfu of Arcanobacterium pyogenes in PBS or with PBS. In Exp. 2, ovariectomy (OVEX) and progesterone treatment were main effects. On d 0, gilts were ovariectomized or a sham procedure was performed. After surgery, gilts received i.m. injections of progesterone (10 mg/5 mL) or 5 mL of safflower oil diluent twice daily. On d 8, gilts were inoculated with the same doses of bacteria as in Exp. 1. In Exp. 1 and 2, vena caval blood was collected for 4 d, after which uteri were collected. Sediment and ability to culture E. coli and A. pyogenes from uterine flushings were used to diagnose infections. Differential white blood cell counts and lymphocyte response to concanavalin A (Con A) and lipopolysaccharides (LPS) were used to measure lymphocyte proliferation. Progesterone, estradiol-17beta, prostaglandin F2alpha, (PGF2alpha), and prostaglandin E2 (PGE2) were measured in vena caval blood. In Exp. 1, d-8 gilts receiving bacteria developed infections, but d-0 gilts receiving bacteria did not. Daily percentages of neutrophils and lymphocytes changed (P < 0.05) with cycle day and bacterial challenge. Basal- and Con A-stimulated lymphocyte proliferation were greater (P < 0.05) for d-0 than for d-8 gilts. Concentrations of PGF2, (P < 0.01) and PGE2 (P < 0.05) increased after bacterial challenge, regardless of stage of the estrous cycle at the time of inoculation. In Exp. 2, OVEX decreased (P < 0.001) and progesterone treatment increased (P < 0.001) progesterone concentrations, and OVEX decreased (P < 0.01) estradiol-17beta. Gilts with ovarian and/or exogenous progesterone developed infections. Daily percentages of neutrophils and lymphocytes changed in response to OVEX, and neutrophils changed (P < 0.05) in response to endogenous and exogenous progesterone. Lymphocyte proliferation in response to Con A and LPS increased (P < 0.05) with OVEX and decreased (P < 0.05) with progesterone treatment. We conclude that endogenous and exogenous progesterone reduce the ability of the uterus in gilts to resist infections.