{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,20]],"date-time":"2026-09-20T18:07:08Z","timestamp":1789927628599,"version":"4.0.1"},"reference-count":52,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2015,11,4]],"date-time":"2015-11-04T00:00:00Z","timestamp":1446595200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Fondo Nacional de Investigaci\u00f3n Cient\u00edfica y Tecnol\u00f3gica","award":["11110076"],"award-info":[{"award-number":["11110076"]}]},{"name":"Fondo Nacional de Investigaci\u00f3n Cient\u00edfica y Tecnol\u00f3gica","award":["1151255"],"award-info":[{"award-number":["1151255"]}]},{"name":"Fondo Nacional de Investigaci\u00f3n Cient\u00edfica y Tecnol\u00f3gica","award":["1130570"],"award-info":[{"award-number":["1130570"]}]},{"name":"Fondo de Investigaci\u00f3n Avanzada en Areas Prioritarias","award":["15130011"],"award-info":[{"award-number":["15130011"]}]},{"name":"RING project ACT 1111"},{"name":"INACH T-19_11"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Periodontal Research"],"published-print":{"date-parts":[[2016,8]]},"abstract":"<jats:sec><jats:title>Background and Objective<\/jats:title><jats:p><jats:italic>Porphyromonas gingivalis<\/jats:italic> infection induces apoptosis inhibition in gingival epithelial cells; however, it is not fully understood which bacterial effectors are involved in this process. The aim of this study is to evaluate whether the <jats:italic>P.\u00a0gingivalis<\/jats:italic> lipopolysaccharide (<jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>), specifically the O\u2010antigen region, affects adherence, invasion, viability and apoptosis of gingival epithelial cells.<\/jats:p><\/jats:sec><jats:sec><jats:title>Material and Methods<\/jats:title><jats:p>Gingival epithelial cells (<jats:styled-content style=\"fixed-case\">OKF<\/jats:styled-content>6\/<jats:styled-content style=\"fixed-case\">TERT<\/jats:styled-content>2 line) were infected by different freshly prepared <jats:italic>P.\u00a0gingivalis<\/jats:italic> clinical isolates, obtained from subjects with chronic periodontitis (<jats:styled-content style=\"fixed-case\">CP<\/jats:styled-content>3 and <jats:styled-content style=\"fixed-case\">CP<\/jats:styled-content>4) and healthy individuals (H1 and H3). Periodontitis and healthy isolates show differences in O\u2010antigen production, as healthy isolates lack the O\u2010antigen region. In addition, cells were infected by a site\u2010specific mutant lacking the O\u2010antigen portion. After 24\u00a0h postinfection, cell proliferation, viability and apoptosis were evaluated by Trypan blue, <jats:styled-content style=\"fixed-case\">MTS<\/jats:styled-content> and annexin V assays, respectively. Bacterial invasion, adhesion and proliferation were measured by gentamicin\/metronidazole protection assays. Finally, toll\u2010like receptor (<jats:styled-content style=\"fixed-case\">TLR)<\/jats:styled-content>2 and <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>4 <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> expression was evaluated by quantitative reverse transcription\u2013polymerase chain reaction. Statistical analysis was performed using <jats:styled-content style=\"fixed-case\">ANOVA<\/jats:styled-content>, Tukey's or Dunnett's tests (<jats:italic>p<\/jats:italic>\u00a0&lt;\u00a00.05).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>At 24\u00a0h postinfection, strains lacking the O\u2010antigen region (healthy isolates and O\u2010antigen ligase\u2010deficient strain) were unable to increase proliferation and viability, or decrease apoptosis as compared with strains producing intact <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content> (periodontitis isolates and reference strain). However, the presence of the O\u2010antigen neither contributed to changes in the ability of the bacteria to adhere to or invade cells, nor to intracellular survival. The presence of O\u2010antigen also increased the expression of <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>4 (nearly sixfold), which correlated with inhibition of apoptosis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>The O\u2010antigen region of <jats:italic>P.\u00a0gingivalis <\/jats:italic><jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content> is required to increase gingival epithelial cell viability upon infection by bacteria and this increase is attributable to a reduction in apoptosis. Moreover, although bacterial internalization is required, the effects observed are not due to alterations in <jats:italic>P.\u00a0gingivalis<\/jats:italic> adherence, invasion or intracellular survival. Interestingly, inhibition of apoptosis correlates with increased <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>4 expression, suggesting a role for <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>4 in this process.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jre.12331","type":"journal-article","created":{"date-parts":[[2015,11,4]],"date-time":"2015-11-04T09:25:01Z","timestamp":1446629101000},"page":"518-528","source":"Crossref","is-referenced-by-count":22,"title":["The <i>Porphyromonas gingivalis<\/i> O antigen is required for inhibition of apoptosis in gingival epithelial cells following bacterial infection"],"prefix":"10.1111","volume":"51","author":[{"given":"C.","family":"Soto","sequence":"first","affiliation":[{"name":"Oral Microbiology Laboratory Department of Pathology and Oral Medicine Faculty of Dentistry Universidad de Chile Santiago Chile"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"I.","family":"Bugue\u00f1o","sequence":"additional","affiliation":[{"name":"Oral Microbiology Laboratory Department of Pathology and Oral Medicine Faculty of Dentistry Universidad de Chile Santiago Chile"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.","family":"Hoare","sequence":"additional","affiliation":[{"name":"Oral Microbiology Laboratory Department of Pathology and Oral Medicine Faculty of Dentistry Universidad de Chile Santiago Chile"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S.","family":"Gonzalez","sequence":"additional","affiliation":[{"name":"Oral Microbiology Laboratory Department of Pathology and Oral Medicine Faculty of Dentistry Universidad de Chile Santiago Chile"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D.","family":"Venegas","sequence":"additional","affiliation":[{"name":"Oral Microbiology Laboratory Department of Pathology and Oral Medicine Faculty of Dentistry Universidad de Chile Santiago Chile"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D.","family":"Salinas","sequence":"additional","affiliation":[{"name":"Oral Microbiology Laboratory Department of Pathology and Oral Medicine Faculty of Dentistry Universidad de Chile Santiago Chile"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S.","family":"Melgar\u2010Rodr\u00edguez","sequence":"additional","affiliation":[{"name":"Laboratory of Periodontal Biology Department of Conservative Dentistry Faculty of Dentistry Universidad de Chile Santiago Chile"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R.","family":"Vernal","sequence":"additional","affiliation":[{"name":"Laboratory of Periodontal Biology Department of Conservative Dentistry Faculty of Dentistry Universidad de Chile Santiago Chile"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J.","family":"Gamonal","sequence":"additional","affiliation":[{"name":"Laboratory of Periodontal Biology Department of Conservative Dentistry Faculty of Dentistry Universidad de Chile Santiago Chile"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A. 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