Uterine response to infectious bacteria in estrous cyclic ewes.

Problem: Luteal-phase uteri are susceptible to infections, and PGE2 and exogenous progesterone can down-regulate, whereas PGF2alpha can up-regulate, uterine immune functions.

Method Of Study: Uteri of follicular- or luteal-phase ewes were inoculated with either saline or bacteria (Arcanobacterium pyogenes and Escherichia colt). Vena caval blood was collected for the next 3 days, and progesterone, PGE2, and PGF2alpha were measured. The effects of 10(-7) M PGE2 (Experiment 1), 10(-7) M PGF2alpha (Experiment 2), 10(-7) M indomethacin (INDO), and diluent on proliferation of lymphocytes from the vena caval blood in response to mitogens was quantified.

Results: Experiment 1: Progesterone was greater (P < 0.01) in luteal than in follicular ewes (3.4 versus 0.4 ng/mL), and only luteal ewes inoculated with bacteria developed infections.Lymphocyte proliferation was least (P = 0.08) in follicular ewes (2.6 versus 4.5 pmol for follicular and luteal, respectively). Concanavalin A (Con A)-stimulated proliferation was less (P < 0.05) for ewes inoculated with bacteria and for cells cultured with diluent (5.9 versus 3.1 pmol for saline and bacteria, respectively) or with INDO (6.6 versus 2.8 pmol for saline and bacteria, respectively). Also, Con A-stimulated lymphocytes from ewes inoculated with bacteria tended to proliferate less (P < 0.1) when cultured with PGE2 (4.9 versus 3.7 pmol for saline and bacteria, respectively) or PGE2 + INDO (5.5 versus 3.8 pmol for saline and bacteria, respectively). Experiment 2: Progesterone was greater (P < 0.01) in luteal than in follicular ewes (6.5 versus 1.2 ng/mL), and only luteal ewes inoculated with bacteria developed infections. Con A-stimulated lymphocyte proliferation was greater (P < 0.001) for follicular ewes (4.1 versus 3.1 pmol for follicular and luteal, respectively). Proliferation of lymphocytes collected from follicular ewes was greater (P < 0.01) when cells were cultured with PGF2alpha (3.5 versus 2.7 pmol for follicular and luteal, respectively), but INDO did not affect unstimulated or mitogen-stimulated proliferation.

Conclusions: Prostaglandin F2alpha enhanced lymphocyte proliferation, whereas bacterial inoculation and in vitro treatment with PGE2 suppressed lymphocyte proliferation. This may signify the involvement of bacterial products and prostaglandins in regulation of uterine immunity.