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Further, the ability of <jats:italic>F.\u00a0nucleatum<\/jats:italic> to invade gingival fibroblasts (<jats:styled-content style=\"fixed-case\">GF<\/jats:styled-content>s) is critical to the development of periodontal diseases. However, the mechanisms underlying the age\u2010related infection of <jats:styled-content style=\"fixed-case\">GF<\/jats:styled-content>s by <jats:italic>F.\u00a0nucleatum<\/jats:italic> remain unknown. We used young (fourth passage) and senescent (22nd passage) <jats:styled-content style=\"fixed-case\">GF<\/jats:styled-content>s to investigate the mechanisms of <jats:italic>F.\u00a0nucleatum<\/jats:italic> infection in aged <jats:styled-content style=\"fixed-case\">GF<\/jats:styled-content>s and first observed increased invasion of <jats:italic>F.\u00a0nucleatum<\/jats:italic> in senescent <jats:styled-content style=\"fixed-case\">GF<\/jats:styled-content>s. We also found that the co\u2010localization of caveolin\u20101 (Cav\u20101), a protein marker of aging, with <jats:italic>F.\u00a0nucleatum<\/jats:italic> and the knockdown of Cav\u20101 in <jats:styled-content style=\"fixed-case\">GF<\/jats:styled-content>s reduced <jats:italic>F.\u00a0nucleatum<\/jats:italic> invasion. Additionally, <jats:italic>F.\u00a0nucleatum<\/jats:italic> infection triggered the production of reactive oxygen species (<jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content>) through activation of <jats:styled-content style=\"fixed-case\">NADPH<\/jats:styled-content> oxidase in <jats:styled-content style=\"fixed-case\">GF<\/jats:styled-content>s, but senescent <jats:styled-content style=\"fixed-case\">GF<\/jats:styled-content>s exhibited significantly lower levels of <jats:styled-content style=\"fixed-case\">NADPH<\/jats:styled-content> oxidase activity and <jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content> production compared with young <jats:styled-content style=\"fixed-case\">GF<\/jats:styled-content>s in both the uninfected and infected conditions. Also, senescent <jats:styled-content style=\"fixed-case\">GF<\/jats:styled-content>s exhibited a decline in proinflammatory cytokine production and extracellular signal regulated kinase (<jats:styled-content style=\"fixed-case\">ERK<\/jats:styled-content>) phosphorylation following <jats:italic>F.\u00a0nucleatum<\/jats:italic> infection. Interestingly, the knockdown of Cav\u20101 in senescent <jats:styled-content style=\"fixed-case\">GF<\/jats:styled-content>s increased <jats:styled-content style=\"fixed-case\">NADPH<\/jats:styled-content> oxidase activity and caused the upregulation of interleukin\u20106 and interleukin\u20108 and the phosphorylation of <jats:styled-content style=\"fixed-case\">ERK<\/jats:styled-content>. Collectively, the increased expression of Cav\u20101 might play a critical role in <jats:italic>F.\u00a0nucleatum<\/jats:italic> invasion and could hinder the host response in senescent <jats:styled-content style=\"fixed-case\">GF<\/jats:styled-content>s.<\/jats:p>","DOI":"10.1111\/omi.12167","type":"journal-article","created":{"date-parts":[[2016,6,17]],"date-time":"2016-06-17T14:46:43Z","timestamp":1466174803000},"page":"236-249","source":"Crossref","is-referenced-by-count":17,"title":["Caveolin\u20101 serves as a negative effector in senescent human gingival fibroblasts during <i>Fusobacterium nucleatum<\/i> infection"],"prefix":"10.1111","volume":"32","author":[{"given":"S.H.","family":"Ahn","sequence":"first","affiliation":[{"name":"Department of Oral Biochemistry Dental Science Research Institute Medical Research Center for Biomineralization Disorders School of Dentistry Chonnam National University Gwangju 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