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We investigated the effect of lipopolysacharide (<jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>) and progesterone (<jats:styled-content style=\"fixed-case\">P<\/jats:styled-content>4) upon expression of <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>\u20104\/<jats:styled-content style=\"fixed-case\">M<\/jats:styled-content>y<jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>88, <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u03b1, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20108, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201010, and <jats:styled-content style=\"fixed-case\">HBD<\/jats:styled-content>2 on the human amniotic epithelium.<\/jats:p><\/jats:sec><jats:sec><jats:title>Method of study<\/jats:title><jats:p>Explants of the human amniotic epithelium were pre\u2010treated with 0.01, 0.1, and 1.0\u00a0\u03bc<jats:sc>m<\/jats:sc> of <jats:styled-content style=\"fixed-case\">P<\/jats:styled-content>4; then cotreated with 1000\u00a0ng\/mL <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>. <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>\u20104 was immuno\u2010detected, and concentrations of <jats:styled-content style=\"fixed-case\">M<\/jats:styled-content>y<jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>88, <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u03b1, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20108, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201010, and <jats:styled-content style=\"fixed-case\">HBD<\/jats:styled-content>2 were quantified by <jats:styled-content style=\"fixed-case\">ELISA<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">P<\/jats:styled-content>4 significantly reduced the expression of <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>\u2010induced <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>\u20104\/<jats:styled-content style=\"fixed-case\">M<\/jats:styled-content>y<jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>88. <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content> increased the concentrations of <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u03b1, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20108, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201010, and <jats:styled-content style=\"fixed-case\">HBD<\/jats:styled-content>2 by factors of 30\u2010, eight, three, three, and fivefold, respectively. P4 at 1.0\u00a0\u03bc<jats:sc>m<\/jats:sc> was the most effective dose to blunt the secretion of <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u03b1, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106, and <jats:styled-content style=\"fixed-case\">HBD<\/jats:styled-content>\u20102. <jats:styled-content style=\"fixed-case\">RU<\/jats:styled-content>\u2010486 blocks the effect of <jats:styled-content style=\"fixed-case\">P<\/jats:styled-content>4.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>P4 inhibited <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>\u2010induced <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>\u20104\/<jats:styled-content style=\"fixed-case\">M<\/jats:styled-content>y<jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>88 and pro\u2010inflammatory factors in the human amniotic epithelium. These results could explain partially how <jats:styled-content style=\"fixed-case\">P<\/jats:styled-content>4 can protect the amniotic region of fetal membranes and generate a compensatory mechanism that limits the secretion of pro\u2010inflammatory modulators, which could jeopardize the immune privilege during pregnancy.<\/jats:p><\/jats:sec>","DOI":"10.1111\/aji.12163","type":"journal-article","created":{"date-parts":[[2013,10,16]],"date-time":"2013-10-16T08:48:55Z","timestamp":1381913335000},"page":"61-72","source":"Crossref","is-referenced-by-count":44,"title":["Progesterone Elicits an Inhibitory Effect upon <scp>LPS<\/scp>\u2010Induced Innate Immune Response in Pre\u2010Labor Human Amniotic Epithelium"],"prefix":"10.1111","volume":"71","author":[{"given":"Pilar","family":"Flores\u2010Espinosa","sequence":"first","affiliation":[{"name":"Department of Cell Biology Instituto Nacional de Perinatolog\u00eda \u2018Isidro Espinosa de los Reyes\u2019 Mexico City Mexico"},{"name":"Posgrado 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