{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T23:40:27Z","timestamp":1791416427529,"version":"4.3.3"},"reference-count":43,"publisher":"American Society for Microbiology","issue":"8","license":[{"start":{"date-parts":[[2014,8,1]],"date-time":"2014-08-01T00:00:00Z","timestamp":1406851200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2014,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Oral microbial communities are extremely complex biofilms with high numbers of bacterial species interacting with each other (and the host) to maintain homeostasis of the system. Disturbance in the oral microbiome homeostasis can lead to either caries or periodontitis, two of the most common human diseases. Periodontitis is a polymicrobial disease caused by the coordinated action of a complex microbial community, which results in inflammation of tissues that support the teeth. It is the most common cause of tooth loss among adults in the United States, and recent studies have suggested that it may increase the risk for systemic conditions such as cardiovascular diseases. In a recent series of papers, Hajishengallis and coworkers proposed the idea of the \u201ckeystone-pathogen\u201d where low-abundance microbial pathogens (\n            <jats:named-content content-type=\"genus-species\">Porphyromonas gingivalis<\/jats:named-content>\n            ) can orchestrate inflammatory disease by turning a benign microbial community into a dysbiotic one. The exact mechanisms by which these pathogens reorganize the healthy oral microbiome are still unknown. In the present manuscript, we present results demonstrating that\n            <jats:named-content content-type=\"genus-species\">P. gingivalis<\/jats:named-content>\n            induces\n            <jats:named-content content-type=\"genus-species\">S. mitis<\/jats:named-content>\n            death and DNA fragmentation in an\n            <jats:italic>in vitro<\/jats:italic>\n            biofilm system. Moreover, we report here the induction of expression of multiple transposases in a\n            <jats:named-content content-type=\"genus-species\">Streptococcus mitis<\/jats:named-content>\n            biofilm when the periodontopathogen\n            <jats:named-content content-type=\"genus-species\">P. gingivalis<\/jats:named-content>\n            is present. Based on these results, we hypothesize that\n            <jats:named-content content-type=\"genus-species\">P. gingivalis<\/jats:named-content>\n            induces\n            <jats:named-content content-type=\"genus-species\">S. mitis<\/jats:named-content>\n            cell death by an unknown mechanism, shaping the oral microbiome to its advantage.\n          <\/jats:p>","DOI":"10.1128\/iai.01976-14","type":"journal-article","created":{"date-parts":[[2014,5,28]],"date-time":"2014-05-28T06:43:50Z","timestamp":1401259430000},"page":"3374-3382","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":36,"title":["The Periodontal Pathogen Porphyromonas gingivalis Induces Expression of Transposases and Cell Death of Streptococcus mitis in a Biofilm Model"],"prefix":"10.1128","volume":"82","author":[{"given":"Ana E.","family":"Duran-Pinedo","sequence":"first","affiliation":[{"name":"Forsyth Institute, Cambridge, Massachusetts, 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