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Tooth slices were inoculated with planktonic cultures of<jats:named-content content-type=\"genus-species\">S. anginosus<\/jats:named-content>or<jats:named-content content-type=\"genus-species\">E. faecalis<\/jats:named-content>alone or in coculture at<jats:named-content content-type=\"genus-species\">S. anginosus<\/jats:named-content>\/<jats:named-content content-type=\"genus-species\">E. faecalis<\/jats:named-content>ratios of 50:50 and 90:10. Attachment was semiquantified by measuring the area covered by fluorescently labeled bacteria. Host response was established by viable histological cell counts, and inflammatory response was measured using reverse transcription-quantitative PCR (RT-qPCR) and immunohistochemistry. A significant reduction in cell viability was observed for single and polymicrobial infections, with no significant differences between infection types (\u223c2,000 cells\/mm<jats:sup>2<\/jats:sup>for infected pulps compared to \u223c4,000 cells\/mm<jats:sup>2<\/jats:sup>for uninfected pulps).<jats:named-content content-type=\"genus-species\">E. faecalis<\/jats:named-content>demonstrated significantly higher levels of attachment (6.5%) than<jats:named-content content-type=\"genus-species\">S. anginosus<\/jats:named-content>alone (2.3%) and mixed-species infections (3.4% for 50:50 and 2.3% for 90:10), with a remarkable affinity for the pulpal vasculature. Infections with<jats:named-content content-type=\"genus-species\">E. faecalis<\/jats:named-content>demonstrated the greatest increase in tumor necrosis factor alpha (TNF-\u03b1) (47.1-fold for<jats:named-content content-type=\"genus-species\">E. faecalis<\/jats:named-content>, 14.6-fold for<jats:named-content content-type=\"genus-species\">S. anginosus<\/jats:named-content>, 60.1-fold for 50:50, and 25.0-fold for 90:10) and interleukin 1\u03b2 (IL-1\u03b2) expression (54.8-fold for<jats:named-content content-type=\"genus-species\">E. faecalis<\/jats:named-content>, 8.8-fold for<jats:named-content content-type=\"genus-species\">S. anginosus<\/jats:named-content>, 54.5-fold for 50:50, and 39.9-fold for 90:10) compared to uninfected samples. Immunohistochemistry confirmed this, with the majority of inflammation localized to the pulpal vasculature and odontoblast regions. Interestingly,<jats:named-content content-type=\"genus-species\">E. faecalis<\/jats:named-content>supernatant and heat-killed<jats:named-content content-type=\"genus-species\">E. faecalis<\/jats:named-content>treatments were unable to induce the same inflammatory response, suggesting<jats:named-content content-type=\"genus-species\">E. faecalis<\/jats:named-content>pathogenicity in pulpitis is linked to its greater ability to attach to the pulpal vasculature.<\/jats:p>","DOI":"10.1128\/iai.00871-17","type":"journal-article","created":{"date-parts":[[2018,2,27]],"date-time":"2018-02-27T11:10:29Z","timestamp":1519729829000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":8,"title":["Enterococcus faecalis Demonstrates Pathogenicity through Increased Attachment in an<i>Ex Vivo<\/i>Polymicrobial Pulpal Infection"],"prefix":"10.1128","volume":"86","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2405-1876","authenticated-orcid":false,"given":"Wayne","family":"Nishio Ayre","sequence":"first","affiliation":[{"name":"School of Dentistry, Cardiff University, Cardiff, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Genevieve","family":"Melling","sequence":"additional","affiliation":[{"name":"School of Dentistry, Cardiff University, Cardiff, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Camille","family":"Cuveillier","sequence":"additional","affiliation":[{"name":"School of Dentistry, Cardiff University, Cardiff, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Madhan","family":"Natarajan","sequence":"additional","affiliation":[{"name":"School of Dentistry, Cardiff University, Cardiff, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jessica L.","family":"Roberts","sequence":"additional","affiliation":[{"name":"School of Dentistry, Cardiff University, Cardiff, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lucy L.","family":"Marsh","sequence":"additional","affiliation":[{"name":"School of Dentistry, Cardiff University, Cardiff, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christopher D.","family":"Lynch","sequence":"additional","affiliation":[{"name":"University Dental School and Hospital, University College Cork, Cork, Ireland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jean-Yves","family":"Maillard","sequence":"additional","affiliation":[{"name":"School of Pharmacy and Pharmaceutical Sciences, Cardiff University, Cardiff, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Stephen P.","family":"Denyer","sequence":"additional","affiliation":[{"name":"School of Pharmacy and Biomolecular Sciences, University of Brighton, Brighton, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alastair J.","family":"Sloan","sequence":"additional","affiliation":[{"name":"School of Dentistry, Cardiff University, Cardiff, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","first-page":"183","volume-title":"Ten cate's oral histology: development, structure, and function","author":"Nanci A","year":"2013","unstructured":"Nanci A. 2013. 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