{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,6,6]],"date-time":"2026-06-06T13:01:31Z","timestamp":1780750891213,"version":"3.54.1"},"posted":{"date-parts":[[2026,6,2]]},"group-title":"Microbiology","reference-count":131,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2026,6,2]],"date-time":"2026-06-02T00:00:00Z","timestamp":1780358400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,6,2]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                <jats:p>\n                  Periodontitis (PD) is a common chronic inflammatory condition and a risk factor for cardiovascular diseases (CVD), yet underlying linking mechanisms remain unclear. The cytokine Oncostain M (OSM) is elevated in both PD and CVD and has emerged as a potential mediator linking oral inflammation to vascular dysfunction. Neutrophils represent a prominent source of OSM during PD and OSM production is elevated by the periodontal pathobiont\n                  <jats:italic>Treponema denticola<\/jats:italic>\n                  (Td). This study investigated the role of exogenous and neutrophil-derived OSM in endothelial cell (EC) dysfunction and the contribution of heterogenous oral\n                  <jats:italic>Treponema<\/jats:italic>\n                  species in OSM production. Human aortic endothelial cells (HAoEC) were used to evaluate the effects of exogenous purified OSM and neutrophil-derived OSM on endothelial cell function. Endothelial permeability, neutrophil transmigration, cytokine production, cell activation and junctional integrity were assessed using transwell assays, ELISAs, real-time PCR, immunoblotting and immunofluorescence microscopy. Exogenous OSM significantly increased HAoEC permeability, neutrophil transmigration and promoted endothelial activation; characterized by increased E-selectin, ICAM-1 and IL-6 expression. Mechanistically, OSM activated OSMR-STAT3 signaling and altered organization of VE-cadherin in adherens junctions and decreased expression of occludin in tight-junctions. Heterogenous oral\n                  <jats:italic>Treponema<\/jats:italic>\n                  species promote OSM production from mouse and human neutrophils in vitro and in vivo using a mouse air pouch model of infection.\n                  <jats:italic>T. denticola<\/jats:italic>\n                  most robustly induced OSM release, likely independent of prominent virulence factors dentilisin and Msp. Co-culture model experiments revealed conditioned media from\n                  <jats:italic>T. denticola<\/jats:italic>\n                  -stimulated neutrophils promoted endothelial cell permeability and IL-6 while reducing endothelial nitric oxide synthase (eNOS) production. These effects were abolished by antibody neutralization of OSM, supporting a casual role of neutrophil-derived OSM. Overall, these findings provide mechanistic insight into putative links between PD and adverse cardiovascular events and identify OSM signaling as critical mediator in inflammation-driven endothelial dysfunction.\n                <\/jats:p>","DOI":"10.64898\/2026.06.01.729434","type":"posted-content","created":{"date-parts":[[2026,6,3]],"date-time":"2026-06-03T05:00:15Z","timestamp":1780462815000},"source":"Crossref","is-referenced-by-count":0,"title":["Neutrophil-Derived Oncostatin M Contributes to Endothelial Cell Dysfunction During\n                  <i>Treponema denticola<\/i>\n                  Interaction"],"prefix":"10.64898","author":[{"given":"Dayron M.","family":"Leyva-Rodriguez","sequence":"first","affiliation":[{"name":"Department of Oral Biology, The State University of New York at Buffalo, Buffalo, NY, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6467-3314","authenticated-orcid":false,"given":"Michelle 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