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Progesterone Elicits an Inhibitory Effect upon LPS ‐Induced Innate Immune Response in Pre‐Labor Human Amniotic Epithelium
Author(s) -
FloresEspinosa Pilar,
PinedaTorres Montzerrat,
VegaSánchez Rodrigo,
EstradaGutiérrez Guadalupe,
EspejelNuñez Aurora,
FloresPliego Arturo,
MaidaClaros Rolando,
ParedesVivas Yuriria,
MoralesMéndez Iyari,
SosaGonzález Irma,
ChávezMendoza Angel,
ZagaClavellina Verónica
Publication year - 2014
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/aji.12163
Subject(s) - innate immune system , epithelium , immune system , tlr2 , secretion , medicine , tumor necrosis factor alpha , endocrinology , immune privilege , inflammation , amnion , amniotic fluid , fetus , chemistry , biology , andrology , immunology , pregnancy , genetics
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 ( P 4) upon expression of TLR ‐4/ M y D 88, TNF α, IL ‐6, IL ‐8, IL ‐10, and HBD 2 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 μ m of P 4; then cotreated with 1000 ng/mL LPS . TLR ‐4 was immuno‐detected, and concentrations of M y D 88, TNF α, IL ‐6, IL ‐8, IL ‐10, and HBD 2 were quantified by ELISA . Results P 4 significantly reduced the expression of LPS ‐induced TLR ‐4/ M y D 88. LPS increased the concentrations of TNF α, IL ‐6, IL ‐8, IL ‐10, and HBD 2 by factors of 30‐, eight, three, three, and fivefold, respectively. P4 at 1.0 μ m was the most effective dose to blunt the secretion of TNF α, IL ‐6, and HBD ‐2. RU ‐486 blocks the effect of P 4. Conclusion P4 inhibited LPS ‐induced TLR ‐4/ M y D 88 and pro‐inflammatory factors in the human amniotic epithelium. These results could explain partially how P 4 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.