TY - JOUR
T1 - Progesterone Elicits an Inhibitory Effect upon LPS-Induced Innate Immune Response in Pre-Labor Human Amniotic Epithelium
AU - Flores-Espinosa, Pilar
AU - Pineda-Torres, Montzerrat
AU - Vega-Sánchez, Rodrigo
AU - Estrada-Gutiérrez, Guadalupe
AU - Espejel-Nuñez, Aurora
AU - Flores-Pliego, Arturo
AU - Maida-Claros, Rolando
AU - Paredes-Vivas, Yuriria
AU - Morales-Méndez, Iyari
AU - Sosa-González, Irma
AU - Chávez-Mendoza, Angel
AU - Zaga-Clavellina, Verónica
PY - 2014/1
Y1 - 2014/1
N2 - 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.
AB - 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.
KW - Chorioamnionitis
KW - Human amniotic epithelium
KW - Inflammation
KW - Innate immunity
KW - Progesterone
KW - TLR-4
UR - http://www.scopus.com/inward/record.url?scp=84890144045&partnerID=8YFLogxK
U2 - 10.1111/aji.12163
DO - 10.1111/aji.12163
M3 - Artículo
SN - 1046-7408
VL - 71
SP - 61
EP - 72
JO - American Journal of Reproductive Immunology
JF - American Journal of Reproductive Immunology
IS - 1
ER -