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Updated: Jun 13, 2026
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Stimulation of Vascular Endothelial Cells Using Neutrophil Extracellular Traps in the Presence of Low-Density Lipoprotein
Published on: August 12, 2025
Neutrophil-Derived Oncostatin M Contributes to Endothelial Cell Dysfunction During Treponema denticola Interaction
Dayron M Leyva-Rodriguez1, Michelle B Visser1
1Department of Oral Biology, The State University of New York at Buffalo, Buffalo, NY, USA.
Biorxiv : the Preprint Server for Biology
|June 12, 2026
Summary
Periodontitis and cardiovascular disease share a link via the cytokine Oncostatin M (OSM). This study shows OSM from neutrophils, boosted by oral bacteria like Treponema denticola, causes endothelial dysfunction, a key factor in cardiovascular events.
Area of Science:
- Biomedical Research
- Oral Health and Systemic Disease
- Inflammation and Immunology
Background:
- Periodontitis (PD) is a chronic inflammatory condition linked to cardiovascular diseases (CVD).
- The cytokine Oncostatin M (OSM) is elevated in both PD and CVD, suggesting a role in connecting oral inflammation to vascular issues.
- Neutrophils are a primary source of OSM in PD, with the oral bacterium Treponema denticola (Td) enhancing OSM production.
Purpose of the Study:
- To investigate the role of exogenous and neutrophil-derived OSM in endothelial cell (EC) dysfunction.
- To determine the contribution of various oral Treponema species in OSM production.
- To elucidate the mechanisms by which OSM mediates inflammation-driven endothelial dysfunction.
Main Methods:
- Human aortic endothelial cells (HAoECs) were used to assess the impact of OSM on endothelial function.
- Assays included transwell for permeability and transmigration, ELISAs and real-time PCR for cytokine and gene expression, and immunoblotting/immunofluorescence for protein and junctional integrity.
- In vivo studies utilized a mouse air pouch model to evaluate OSM production by neutrophils stimulated by Treponema species.
Main Results:
- Exogenous and neutrophil-derived OSM significantly increased endothelial permeability, neutrophil transmigration, and EC activation (E-selectin, ICAM-1, IL-6).
- OSM activated the OSMR-STAT3 signaling pathway, disrupted VE-cadherin in adherens junctions, and reduced occludin in tight junctions.
- Oral Treponema species, particularly T. denticola, stimulated neutrophils to produce OSM, which mediated increased permeability and IL-6 production while decreasing eNOS in ECs.
Conclusions:
- Neutrophil-derived OSM, induced by oral bacteria, plays a critical role in endothelial dysfunction.
- OSM signaling is a key mediator linking periodontitis-associated inflammation to cardiovascular disease risk.
- Targeting OSM signaling may offer a therapeutic strategy for managing cardiovascular complications of periodontitis.
