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  • Title: Progesterone elicits an inhibitory effect upon LPS-induced innate immune response in pre-labor human amniotic epithelium.
    Author: Flores-Espinosa P, Pineda-Torres M, Vega-Sánchez R, Estrada-Gutiérrez G, Espejel-Nuñez A, Flores-Pliego A, Maida-Claros R, Paredes-Vivas Y, Morales-Méndez I, Sosa-González I, Chávez-Mendoza A, Zaga-Clavellina V.
    Journal: Am J Reprod Immunol; 2014 Jan; 71(1):61-72. PubMed ID: 24128422.
    Abstract:
    PROBLEM: Infection of human fetal membranes elicits secretion of pro-inflammatory modulators through its innate immune capacities. We investigated the effect of lipopolysacharide (LPS) and progesterone (P4) upon expression of TLR-4/MyD88, TNFα, IL-6, IL-8, IL-10, and HBD2 on the human amniotic epithelium. METHOD OF STUDY: Explants of the human amniotic epithelium were pre-treated with 0.01, 0.1, and 1.0 μM of P4; then cotreated with 1000 ng/mL LPS. TLR-4 was immuno-detected, and concentrations of MyD88, TNFα, IL-6, IL-8, IL-10, and HBD2 were quantified by ELISA. RESULTS: P4 significantly reduced the expression of LPS-induced TLR-4/MyD88. LPS increased the concentrations of TNFα, IL-6, IL-8, IL-10, and HBD2 by factors of 30-, eight, three, three, and fivefold, respectively. P4 at 1.0 μM was the most effective dose to blunt the secretion of TNFα, IL-6, and HBD-2. RU-486 blocks the effect of P4. CONCLUSION: P4 inhibited LPS-induced TLR-4/MyD88 and pro-inflammatory factors in the human amniotic epithelium. These results could explain partially how P4 can protect the amniotic region of fetal membranes and generate a compensatory mechanism that limits the secretion of pro-inflammatory modulators, which could jeopardize the immune privilege during pregnancy.
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