American journal of reproductive immunology (New York, N.Y. : 1989) · 2013
Progesterone elicits an inhibitory effect upon LPS-induced innate immune response in pre-labor human amniotic epithelium.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Flores-Espinosa Pilar, Pineda-Torres Montzerrat, Vega-Sánchez Rodrigo, Estrada-Gutiérrez Guadalupe, Espejel-Nuñez Aurora, Flores-Pliego Arturo, Maida-Claros Rolando, Paredes-Vivas Yuriria, Morales-Méndez Iyari, Sosa-González Irma, Chávez-Mendoza Angel, Zaga-Clavellina Verónica
Аннотация
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.
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.