{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,23]],"date-time":"2026-07-23T23:11:26Z","timestamp":1784848286242,"version":"3.55.0"},"reference-count":41,"publisher":"American Society for Microbiology","issue":"5","license":[{"start":{"date-parts":[[2025,5,13]],"date-time":"2025-05-13T00:00:00Z","timestamp":1747094400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2025,5,13]],"date-time":"2025-05-13T00:00:00Z","timestamp":1747094400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/100000072","name":"National Institute of Dental and Craniofacial Research","doi-asserted-by":"publisher","award":["R03DE032392"],"award-info":[{"award-number":["R03DE032392"]}],"id":[{"id":"10.13039\/100000072","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000072","name":"National Institute of Dental and Craniofacial Research","doi-asserted-by":"publisher","award":["R01 DE029497"],"award-info":[{"award-number":["R01 DE029497"]}],"id":[{"id":"10.13039\/100000072","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2025,5,13]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:sec>\n            <jats:title\/>\n            <jats:p>\n              The oral bacterium\n              <jats:italic toggle=\"yes\">Tannerella forsythia<\/jats:italic>\n              is associated with periodontitis, an inflammatory disease affecting tooth-supporting tissues. The bacterium produces a dicarbonyl compound, methylglyoxal (MGO), whose levels correlate with the severity of periodontitis. MGO can induce inflammation directly or via the generation of glycation products called advanced glycation end products (AGEs).\n              <jats:italic toggle=\"yes\">T. forsythia<\/jats:italic>\n              -produced MGO has been shown to cause tissue collagen glycation, which in turn can induce pro-inflammatory cytokine secretion in monocytes via receptor for advanced glycation end product (RAGE) receptor activation. The current study investigated the impact of\n              <jats:italic toggle=\"yes\">T. forsythia<\/jats:italic>\n              -secreted MGO on human gingival fibroblasts and endothelial cells. For assessing the\n              <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n              impact of\n              <jats:italic toggle=\"yes\">T. forsythia<\/jats:italic>\n              -secreted MGO, we employed an oral gavage-induced mouse model of periodontitis utilizing the wild-type and MGO-deficient strains of\n              <jats:italic toggle=\"yes\">T. forsythia<\/jats:italic>\n              . Our results showed that the apoptotic activity was enhanced, and cell migration was reduced in fibroblasts exposed to collagen treated with the\n              <jats:italic toggle=\"yes\">T. forsythia<\/jats:italic>\n              wild-type culture supernatant. Moreover, monocyte binding, reactive oxygen species production, and inflammatory cytokine secretion were increased in fibroblasts, and neutrophil transendothelial migration was enhanced in response to the\n              <jats:italic toggle=\"yes\">T. forsythia<\/jats:italic>\n              wild type-treated collagen.\n              <jats:italic toggle=\"yes\">In vivo<\/jats:italic>\n              , increased AGE accumulation in gingival tissues with increased alveolar bone loss was observed in wild-type\n              <jats:italic toggle=\"yes\">T. forsythia<\/jats:italic>\n              as compared to the MGO-deficient strain-infected mice. These data demonstrated that\n              <jats:italic toggle=\"yes\">T. forsythia<\/jats:italic>\n              -secreted MGO contributes to periodontal tissue destruction by mitigating gingival fibroblast-mediated tissue healing and promoting endothelial cell dysfunction. These findings provide a basis for targeting the\n              <jats:italic toggle=\"yes\">T. forsythia<\/jats:italic>\n              -associated AGE-RAGE axis in alleviating periodontitis.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1128\/iai.00560-24","type":"journal-article","created":{"date-parts":[[2025,4,4]],"date-time":"2025-04-04T09:31:23Z","timestamp":1743759083000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":8,"title":["Oral bacterium contributes to periodontal inflammation by forming advanced glycation end products"],"prefix":"10.1128","volume":"93","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3577-7675","authenticated-orcid":true,"given":"Rajendra P.","family":"Settem","sequence":"first","affiliation":[{"name":"Department of Oral Biology, School of Dental Medicine, University at Buffalo","place":["Buffalo, 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