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dc.contributor.authorEdwards, V.L.
dc.contributor.authorSmith, S.B.
dc.contributor.authorMcComb, E.J.
dc.contributor.authorHumphrys, M.S.
dc.contributor.authorGajer, P.
dc.contributor.authorGwilliam, K.
dc.contributor.authorTerplan, M.
dc.contributor.authorMark, K.S.
dc.contributor.authorBrotman, R.M.
dc.contributor.authorBavoil, P.M.
dc.contributor.authorRavela, J.
dc.contributor.authorBing, M.en_US
dc.date.accessioned2019-09-10T17:30:15Z
dc.date.available2019-09-10T17:30:15Z
dc.date.issued2019
dc.identifier.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85071282597&doi=10.1128%2fmBio.01548-19&partnerID=40&md5=b4405733dba806f10d68402017b2d1fc
dc.identifier.urihttp://hdl.handle.net/10713/10493
dc.description.abstractThe mechanism(s) by which Lactobacillus-dominated cervicovaginal microbiota provide a barrier to Chlamydia trachomatis infection remain(s) unknown. Here we evaluate the impact of different Lactobacillus spp. identified via cultureindependent metataxonomic analysis of C. trachomatis-infected women on C. trachomatis infection in a three-dimensional (3D) cervical epithelium model. Lactobacillus spp. that specifically produce D(-) lactic acid were associated with long-term protection against C. trachomatis infection, consistent with reduced protection associated with Lactobacillus iners, which does not produce this isoform, and with decreased epithelial cell proliferation, consistent with the observed prolonged protective effect. Transcriptomic analysis revealed that epigenetic modifications involving histone deacetylase-controlled pathways are integral to the cross talk between host and microbiota. These results highlight a fundamental mechanism whereby the cervicovaginal microbiota modulates host functions to protect against C. trachomatis infection. IMPORTANCE The vaginal microbiota is believed to protect women against Chlamydia trachomatis, the etiologic agent of the most prevalent sexually transmitted infection (STI) in developed countries. The mechanism underlying this protection has remained elusive. Here, we reveal the comprehensive strategy by which the cervicovaginal microbiota modulates host functions to protect against chlamydial infection, thereby providing a novel conceptual mechanistic understanding. Major implications of this work are that (i) the impact of the vaginal microbiota on the epithelium should be considered in future studies of chlamydial infection and other STIs and (ii) a fundamental understanding of the cervicovaginal microbiota’s role in protection against STIs may enable the development of novel microbiome-based therapeutic strategies to protect women from infection and improve vaginal and cervical health. Copyright 2019 Edwards et al.en_US
dc.description.sponsorshipResearch reported in this publication was supported by the National Institute for Allergy and Infectious Diseases of the National Institutes of Health under award numbers U19AI084044 and UH2AI083264.en_US
dc.description.urihttps://doi.org/10.1128/mBio.01548-19en_US
dc.language.isoen-USen_US
dc.publisherAmerican Society for Microbiologyen_US
dc.relation.ispartofmBio
dc.subjectEpigeneticen_US
dc.subjectLactic aciden_US
dc.subjectLactobacillusen_US
dc.subjectMicrobiomeen_US
dc.subjectProliferationen_US
dc.subjectSexually transmitted infectionen_US
dc.titleThe cervicovaginal microbiota-host interaction modulates chlamydia trachomatis infectionen_US
dc.typeArticleen_US
dc.identifier.doi10.1128/mBio.01548-19
dc.identifier.pmid31409678


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