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• W1963558739 abstract "Objective Progesterone supplementation has been shown to be efficacious in preventing preterm birth. We sought to investigate the effects of progesterone on fetal inflammatory responses. Study Design Fetal mononuclear cells were isolated from umbilical cord blood and exposed to vehicle or progesterone (P4) for 1 hour prior to lipopolysaccharide (LPS) stimulation. Supernatants were assayed for tumor necrosis factor-α. Similar experiments were performed using cyclic adenosine monophosphate (cAMP) and progesterone modulators. The effect of P4 treatment on intracellular cAMP levels was also determined. Results LPS treatment led to a significant increase in cytokine production by fetal mononuclear cells. Despite the lack of detectable nuclear progesterone receptors, P4 suppressed this inflammatory response. R5020 (progesterone agonist), forskolin (cAMP inducer), and dibutyryl cAMP (cAMP agonist) all achieved immunosuppression. The cAMP antagonist, Rp-cAMP, blocked the inhibitory effect of progesterone. P4 significantly increased intracellular cAMP levels. Conclusion Progesterone rapidly suppresses the fetal inflammatory response, possibly via nongenomic activation of the cAMP cascade. Progesterone supplementation has been shown to be efficacious in preventing preterm birth. We sought to investigate the effects of progesterone on fetal inflammatory responses. Fetal mononuclear cells were isolated from umbilical cord blood and exposed to vehicle or progesterone (P4) for 1 hour prior to lipopolysaccharide (LPS) stimulation. Supernatants were assayed for tumor necrosis factor-α. Similar experiments were performed using cyclic adenosine monophosphate (cAMP) and progesterone modulators. The effect of P4 treatment on intracellular cAMP levels was also determined. LPS treatment led to a significant increase in cytokine production by fetal mononuclear cells. Despite the lack of detectable nuclear progesterone receptors, P4 suppressed this inflammatory response. R5020 (progesterone agonist), forskolin (cAMP inducer), and dibutyryl cAMP (cAMP agonist) all achieved immunosuppression. The cAMP antagonist, Rp-cAMP, blocked the inhibitory effect of progesterone. P4 significantly increased intracellular cAMP levels. Progesterone rapidly suppresses the fetal inflammatory response, possibly via nongenomic activation of the cAMP cascade." @default.
• W1963558739 created "2016-06-24" @default.
• W1963558739 creator A5020861250 @default.
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• W1963558739 creator A5070738880 @default.
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• W1963558739 date "2009-08-01" @default.
• W1963558739 modified "2023-09-24" @default.
• W1963558739 title "Progesterone suppresses the fetal inflammatory response ex vivo" @default.
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• W1963558739 doi "https://doi.org/10.1016/j.ajog.2009.05.012" @default.
• W1963558739 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19646573" @default.
• W1963558739 hasPublicationYear "2009" @default.
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