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Therefore, in this study we investigated the strain\u2010specific immune response using a murine experimental model of periodontitis. Periodontitis was induced by <jats:italic><jats:styled-content style=\"fixed-case\">P<\/jats:styled-content>.\u00a0gingivalis<\/jats:italic> strains <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>7<jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>1\u201028, <jats:styled-content style=\"fixed-case\">W<\/jats:styled-content>83 and <jats:styled-content style=\"fixed-case\">W<\/jats:styled-content>50, and later confirmed by the presence of <jats:italic><jats:styled-content style=\"fixed-case\">P<\/jats:styled-content>.\u00a0gingivalis<\/jats:italic> in the oral microflora and by alveolar bone resorption. Splenocytes were evaluated for gene expression, cellular proteins and cytokine expression. Dendritic cells were stimulated <jats:italic>in vitro<\/jats:italic> for <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content> helper cell\u2013cytokine profiling. Results showed that <jats:italic><jats:styled-content style=\"fixed-case\">P<\/jats:styled-content>.\u00a0gingivalis<\/jats:italic> had the ability to alter the systemic immune response after bacterial exposure. Strains <jats:styled-content style=\"fixed-case\">W<\/jats:styled-content>50 and <jats:styled-content style=\"fixed-case\">W<\/jats:styled-content>83 were shown to induce alveolar bone loss, whereas the <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>7<jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>1\u201028 strain did not significantly promote bone resorption in mice. Splenocytes derived from mice infected with strains <jats:styled-content style=\"fixed-case\">W<\/jats:styled-content>50 and <jats:styled-content style=\"fixed-case\">W<\/jats:styled-content>83 induced expression of high levels of interleukin\u20104 (<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20104) but <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>7<jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>1\u201028 stimulated increased <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201010. Stimulation of dendritic cells <jats:italic>in vitro<\/jats:italic> showed a similar pattern of cytokine expression of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201012p40, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106 and transforming growth factor\u2010\u03b2 among strains. A distinct systemic response <jats:italic>in vivo<\/jats:italic> was observed among different strains of <jats:italic><jats:styled-content style=\"fixed-case\">P<\/jats:styled-content>.\u00a0gingivalis,<\/jats:italic> with <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201010 associated with the least amount of alveolar bone loss. Evaluation of pathogen\u2010driven systemic immune responses associated with periodontal disease pathogenesis may assist in defining how periodontitis may impact other diseases.<\/jats:p>","DOI":"10.1111\/omi.12001","type":"journal-article","created":{"date-parts":[[2012,9,18]],"date-time":"2012-09-18T09:37:10Z","timestamp":1347961030000},"page":"483-495","source":"Crossref","is-referenced-by-count":24,"title":["Divergence of the systemic immune response following oral infection with distinct strains of <i><scp>P<\/scp>orphyromonas gingivalis<\/i>"],"prefix":"10.1111","volume":"27","author":[{"given":"J.T.","family":"Marchesan","sequence":"first","affiliation":[{"name":"Department of Periodontics and Oral Medicine University of Michigan School of Dentistry Ann Arbor MI USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T.","family":"Morelli","sequence":"additional","affiliation":[{"name":"Department of Periodontics and Oral Medicine University of Michigan School of 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