P.G-OMV Promote Endothelial Cell Inflammatory Response And Dysfunction.

Porphyromonas gingivalis (P. gingivalis), a key periodontal pathogen, is implicated in atherosclerosis pathogenesis.P.gingivalis-derived OMV (P.g-OMV)resist degradation and evade antibiotics, yet their impact on atherosclerosis remains elusive. This study investigates the pathogenic mechanisms of P.g-OMV in atherosclerosis and their resistance to antibiotic suppression, aiming to provide insights into overcoming therapeutic limitations P.g-OMV from various sources were isolated and characterized using TEM, SEM, BCA protein assay, NanoFCM for concentration/size analysis, Western blot, and proteomics to compare protein composition. HUVECs (passages 3–5) were divided into control, 10 μg/mL P.g-OMV, and 10 μg/mL MTZ+P.g-OMV groups. Pro-inflammatory effects and dysfunction induced by P.g-OMV were evaluated via CCK-8, ELISA, Western blot, fluorescent probes, and transcriptomics. SEM, TEM, NanoFCM, and BCA assays revealed a 2.3-fold increase in P.g-OMV production and enlarged vesicle size after treatment with the minimum inhibitory concentration of MTZ. Proteomic analysis identified antibiotic-induced upregulation of resistance-related proteins in P.g-OMV. Western blot, ELISA, and transcriptomic data demonstrated that P.g-OMV from different sources activated the TLR2/NF-κB signaling pathway, promoting inflammation and dysfunction in HUVECs P.g-OMV promote HUVEC inflammation and dysfunction via TLR2/NF-κB, evading antibiotic suppression. Antibiotic stress enhances OMV pathogenicity, highlighting limitations of conventional therapies in mitigating systemic effects of P. gingivalis