{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T02:39:47Z","timestamp":1772159987366,"version":"3.50.1"},"reference-count":51,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2013,11,11]],"date-time":"2013-11-11T00:00:00Z","timestamp":1384128000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American J Rep Immunol"],"published-print":{"date-parts":[[2014,2]]},"abstract":"\n Problem<\/jats:title>\n \n Susceptibility to\n \n C<\/jats:styled-content>\n hlamydia trachomatis\n <\/jats:italic>\n infection is increased by oral contraceptives and modulated by sex hormones. We therefore sought to determine the effects of female sex hormones on the innate immune response to\n \n C<\/jats:styled-content>\n .\u00a0trachomatis\n <\/jats:italic>\n infection.\n <\/jats:p>\n <\/jats:sec>\n \n Method of study<\/jats:title>\n \n ECC<\/jats:styled-content>\n \u20101 endometrial cells, pre\u2010treated with oestradiol or progesterone, were infected with\n \n C<\/jats:styled-content>\n .\u00a0trachomatis\n <\/jats:italic>\n and the host transcriptome analysed by\n I<\/jats:styled-content>\n llumina\n S<\/jats:styled-content>\n entrix\n H<\/jats:styled-content>\n uman\n R<\/jats:styled-content>\n ef\u20108 microarray. Primary endocervical epithelial cells, prepared at either the proliferative or secretory phase of the menstrual cycle, were infected with\n C.\u00a0trachomatis<\/jats:italic>\n and cytokine gene expression determined by quantitative\n RT<\/jats:styled-content>\n \u2010\n PCR<\/jats:styled-content>\n analysis.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n Chlamydia trachomatis<\/jats:italic>\n yield from progesterone\u2010primed\n ECC<\/jats:styled-content>\n \u20101 cells was significantly reduced compared with oestradiol\u2010treated cells. Genes upregulated in progesterone\u2010treated and\n \n C<\/jats:styled-content>\n hlamydia\n <\/jats:italic>\n \u2010infected cells only included multiple\n CC<\/jats:styled-content>\n and\n CXC<\/jats:styled-content>\n chemokines,\n IL<\/jats:styled-content>\n \u201017C,\n IL<\/jats:styled-content>\n \u201029,\n IL<\/jats:styled-content>\n \u201032,\n TNF<\/jats:styled-content>\n \u2010\u03b1,\n DEFB<\/jats:styled-content>\n 4B,\n LCN<\/jats:styled-content>\n 2,\n S<\/jats:styled-content>\n 100\n A<\/jats:styled-content>\n 7\u20109,\n ITGAM<\/jats:styled-content>\n ,\n NOD<\/jats:styled-content>\n 2,\n JAK<\/jats:styled-content>\n 1,\n IL<\/jats:styled-content>\n \u20106\n ST<\/jats:styled-content>\n , type\n I<\/jats:styled-content>\n and\n II<\/jats:styled-content>\n interferon receptors, numerous interferon\u2010stimulated genes and\n STAT<\/jats:styled-content>\n 6.\n CXCL<\/jats:styled-content>\n 10,\n CXCL<\/jats:styled-content>\n 11,\n CX<\/jats:styled-content>\n 3<\/jats:sub>\n CL<\/jats:styled-content>\n 1 and\n IL<\/jats:styled-content>\n \u201017\n C<\/jats:styled-content>\n , which were also upregulated in infected secretory\u2010stage primary cells, and there was a trend towards higher levels of immune mediators in infected secretory\u2010phase compared with proliferative\u2010phase cells.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusion<\/jats:title>\n Progesterone treatment primes multiple innate immune pathways in hormone\u2010responsive epithelial cells that could potentially increase resistance to chlamydial infection.<\/jats:p>\n <\/jats:sec>","DOI":"10.1111\/aji.12168","type":"journal-article","created":{"date-parts":[[2013,11,11]],"date-time":"2013-11-11T03:42:41Z","timestamp":1384141361000},"page":"165-177","source":"Crossref","is-referenced-by-count":29,"title":["Progesterone Activates Multiple Innate Immune Pathways in\n \n C<\/scp>\n hlamydia trachomatis\n <\/i>\n \u2010Infected Endocervical 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