{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T05:01:52Z","timestamp":1773291712441,"version":"3.50.1"},"reference-count":28,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2009,3,13]],"date-time":"2009-03-13T00:00:00Z","timestamp":1236902400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Periodontal Research"],"published-print":{"date-parts":[[2009,8]]},"abstract":"<jats:p><jats:bold>Background and Objective:\u2002<\/jats:bold> Local persistent infection by <jats:italic>Porphyromonas gingivalis<\/jats:italic> leads to inflammatory systemic diseases, such as atherosclerosis. We have reported previously that avirulent <jats:italic>P.\u2003gingivalis<\/jats:italic> fimbriae\u2010dependent invasion into endothelial cells might be involved in progression of atherosclerosis. Although interleukin\u20106 (IL\u20106) regulates progression of atherosclerosis, little is known about the relationship of <jats:italic>P.\u2003gingivalis<\/jats:italic> fimbriae\u2010dependent invasion to IL\u20106 regulation in endothelial cells.<\/jats:p><jats:p><jats:bold>Material and Methods:\u2002<\/jats:bold> We examined the secretion of IL\u20106 and the expression of the IL\u20106 signal transducer gp130 in human umbilical vein endothelial cells (HUVEC) infected with the wild\u2010type FDC381 strain of <jats:italic>P.\u2003gingivalis<\/jats:italic>and a fimbriae\u2010deficient mutant (<jats:italic>fimA<\/jats:italic>) by enzyme\u2010linked immunosorbent assay, quantitative reverse transcriptase\u2010polymerase chain reaction (RT\u2010PCR) and flow cytometry (fluorescence\u2010activated cell sorting, FACS) analysis.<\/jats:p><jats:p><jats:bold>Results:\u2002<\/jats:bold> Coculture of HUVEC with <jats:italic>P.\u2003gingivalis<\/jats:italic> resulted in increase of IL\u20106 secretion at 24\u2003h postinfection. Interestingly, the increase was inhibited significantly in HUVEC infected with the <jats:italic>P.\u2003gingivalis fimA<\/jats:italic> mutant. In addition, the increase of IL\u20106 secretion induced by <jats:italic>P.\u2003gingivalis<\/jats:italic> infection was significantly impaired by the meiosis specific kinase 1 inhibitor, PD98059, or the nuclear factor\u2003\u03baB inhibitor, Bay11\u20107082. Furthermore, we demonstrated that gp130 expression increased with <jats:italic>P.\u2003gingivalis<\/jats:italic> infection. Importantly, gp130 expression was significantly impaired by <jats:italic>P\u00a0gingivalis fimA<\/jats:italic> mutant infection compared with wild\u2010type <jats:italic>P.\u2003gingivalis<\/jats:italic> infection, as assessed by both quantitative RT\u2010PCR and FACS analysis.<\/jats:p><jats:p><jats:bold>Conclusion:\u2002<\/jats:bold> Our findings indicate that <jats:italic>P.\u2003gingivalis<\/jats:italic> fimbriae are important factors in the autocrine regulation of IL\u20106, by increasing gp130 in endothelial cells.<\/jats:p>","DOI":"10.1111\/j.1600-0765.2008.01150.x","type":"journal-article","created":{"date-parts":[[2009,3,13]],"date-time":"2009-03-13T10:08:31Z","timestamp":1236938911000},"page":"550-556","source":"Crossref","is-referenced-by-count":9,"title":["<i>Porphyromonas gingivalis<\/i> fimbriae\u2010dependent interleukin\u20106 autocrine regulation by increase of gp130 in endothelial 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