Does exogeneous progestogen alter the relationships among PGF2α, 13,14-dihydro-15-keto-PGF2α, progesterone, and estrogens in ovarian-intact ewes around the time of luteolysis?

Fortin, S.S.; Sayre, B.L.; Lewis, Gregory S.

doi:10.1016/0090-6980(94)90059-0

Cited by 16 publications

(15 citation statements)

References 33 publications

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“…Ovarian steroids, especially progesterone, regulate uterine prostaglandin synthesis 10 . Prostanoids, particularly leukotrienes and two‐series prostaglandins, are potent immunomodulatory molecules 11–13 .…”

Section: Introductionmentioning

confidence: 99%

Modulation of the Uterine Response to Infectious Bacteria in Postpartum Ewes

Seals¹,

Wulster-Radcliffe²,

Lewis³

2002

American J Rep Immunol

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Section: Introductionmentioning

confidence: 99%

Modulation of the Uterine Response to Infectious Bacteria in Postpartum Ewes

Seals¹,

Wulster-Radcliffe²,

Lewis³

2002

American J Rep Immunol

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“…pulses resulting from the administration of onapristone is consistent with the findings that the administration of exogenous progestogens at the time of luteolysis reduced the amplitude of PGF 2 . pulses [54,55]. Progesterone withdrawal in response to ovariectomy [56,57] or during spontaneous luteolysis [39,46,47] was associated with an increase in the frequency of PGF2, secretion.…”

Section: Discussionmentioning

confidence: 92%

Influence of Estradiol and Progesterone withdrawal on the Secretion of and the Temporal Correlation between Pulses of Oxytocin and Prostaglandin F2α, in Ewes1

Walker¹,

Weston²,

Hixon³

1997

Biology of Reproduction

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The primary objective was to examine the effects of estradiol and the progesterone receptor antagonist onapristone on the pulsatile secretion of prostaglandin F(2alpha) (PGF(2alpha)) and ovarian and pituitary oxytocin. A 2 x 2 factorial arrangement of estradiol and onapristone treatments was administered to groups of 5 ewes after destruction of ovarian follicles on Day 8 of the cycle. Estradiol treatments consisted of the administration of a silicone elastomer implant, either containing or not containing estradiol, on Day 8 plus 50 microg of estradiol or corn oil on Days 11 and 12. Onapristone (2 mg/kg) or its vehicle were administered on Day 13, immediately preceding the simultaneous collection of blood samples from the carotid artery, jugular vein, and vena cava at 7.5-min intervals for 7 h. Ewes were immediately killed for measurements of uterine oxytocin receptor concentrations and phosphatidylinositide turnover. More oxytocin pulses were detected in the jugular vein than in the carotid artery (p < 0.01), suggesting that the pituitary is a source of oxytocin. A similar number (p > 0.1) of PGF(2alpha) pulses were correlated with oxytocin pulses as were not. The linked PGF(2alpha) pulses were longer in duration (p = 0.01) with a tendency toward a higher amplitude (p = 0.08). The corresponding vena caval oxytocin pulses had a longer duration (p = 0.02) than those not linked to PGF(2alpha). Estradiol increased oxytocin receptor concentrations and the turnover of phosphatidylinositides (p = 0.02) without affecting PGF(2alpha) pulse characteristics. Onapristone increased (p = 0.03) PGF(2alpha) pulse amplitude. Although a lower than expected temporal correlation between oxytocin and PGF(2alpha) pulses was observed, the distinguishing characteristics of linked pulses may be indicative of their physiological significance.

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“…Vena caval blood was collected through catheters that were positioned just cranial to the entry of uteroovarian blood [30]. Indeed, 6α-methyl-17α-hydroxyprogesterone acetate (a progestogen commonly used to control the estrous cycle) reduced uterine secretion of PGF 2α [31]. Ovariectomy increased and exogenous progesterone decreased Con A-stimulated lymphocyte proliferation, and ovariectomy increased LPS-stimulated lymphocyte proliferation [17].…”

Section: Reviewmentioning

confidence: 99%

“…13,14-Dihydro-15-keto-PGF 2α is a metabolite of PGF 2α with a half-life of approximately 15 min, compared with approximately 1 min for PGF 2α [37,38]. During the postpartum period, jugular concentrations of PGFM are a close reflection of uterine secretion of PGF 2α ; however, that does not seem to be the case during the estrous cycle, when the uterus produces considerably less PGF 2α [31,37,39]. The results of studies with postpartum dairy cows indicated that PGFM concentrations were less in cows that later developed uterine infections than they were in cows that did not develop uterine infections [15,36].…”

Section: Reviewmentioning

confidence: 99%

Steroidal regulation of uterine resistance to bacterial infection in livestock

Lewis

2003

Reprod Biol Endocrinol

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Postpartum uterine infections reduce reproductive efficiency and have significant animal welfare and economic consequences. Postpartum uterine infections are classified as nonspecific, but Arcanobacterium pyogenes and Escherichia coli are usually associated with them in cattle and sheep. Pyometra is the most common type of uterine infection in dairy cattle, and it is detected almost exclusively in cows with active corpora lutea. Luteal progesterone typically down-regulates uterine immune functions and prevents the uterus from resisting infections. Progesterone also can down-regulate uterine eicosanoid synthesis. This seems to be a critical event in the onset of uterine infections, because eicosanoids can up-regulate immune cell functions in vitro. In addition, exogenous prostaglandin F2 alpha stimulates uterine secretion of prostaglandin F2 alpha and enhances immune functions in vivo. Thus, one may hypothesize that eicosanoids can override the negative effects of progesterone and that the up-regulatory effects of exogenous prostaglandin F2 alpha allow the uterus to resolve an infection, regardless of progesterone concentrations. Based on the results of studies to test that hypothesis, cows, sheep, and pigs in various physiological statuses are resistant to intrauterine infusions of Arcanobacterium pyogenes and Escherichia coli, unless progesterone concentrations are increased. In sheep and pigs, exogenous prostaglandin F2 alpha stimulates uterine production of prostaglandin F2 alpha and allows the uterus to resolve Arcanobacterium pyogenes-Escherichia coli-induced infections, even when progesterone is maintained at luteal phase concentrations before and after treatment. Prostaglandin F2 alpha is a proinflammatory molecule that stimulates the production of various proinflammatory cytokines, and it may enhance uterine production of leukotriene B4. Proinflammatory cytokines and leukotriene B4 enhance phagocytosis and lymphocyte functions. Even though there are clear associations among prostaglandin F2 alpha, leukotriene B4, proinflammatory cytokines, phagocytosis, and lymphocyte functions, the mechanism of action of exogenous prostaglandin F2 alpha in overriding the down-regulatory effects of progesterone and resolving uterine infections has not been elucidated. Defining this mechanism should yield new prevention and treatment strategies for uterine infections that do not rely on antibiotic and antimicrobial compounds.

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Does exogeneous progestogen alter the relationships among PGF2α, 13,14-dihydro-15-keto-PGF2α, progesterone, and estrogens in ovarian-intact ewes around the time of luteolysis?

Cited by 16 publications

References 33 publications

Modulation of the Uterine Response to Infectious Bacteria in Postpartum Ewes

Modulation of the Uterine Response to Infectious Bacteria in Postpartum Ewes

Influence of Estradiol and Progesterone withdrawal on the Secretion of and the Temporal Correlation between Pulses of Oxytocin and Prostaglandin F2α, in Ewes1

Steroidal regulation of uterine resistance to bacterial infection in livestock

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