ArticleBMC oral health2026
Porphyromonas gingivalis outer membrane vesicles drive neuroinflammation via TGM2-mediated mitochondria-associated endoplasmic reticulum membranes.
Article in BMC oral health, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundPorphyromonas gingivalis (P.g), a key periodontal pathogen, is implicated in Alzheimer's disease (AD). Given that mitochondrial dysfunction is a common event happened in neurodegenerative diseases, mitochondria-associated endoplasmic reticulum (ER) membranes (MAMs) play a potential role in AD pathology. This study aimed to investigate the impact of P.g derived outer membrane vesicles (P.g-OMVs) on neuroinflammation in the onset and progression of AD, and to elucidate the underlying mechanism.
methodsEight-week-old male C57BL/6 mice received bilateral gingival injections of P.g-OMVs (4 × 10⁸ particles) 3 times weekly for 8 weeks to assess cognitive impairment and neuroinflammation. RNA-seq identified differentially expressed genes (DEGs) and enriched pathway in brain tissues. In vitro, HT22 cells were treated with P.g-OMVs (5 µg/mL), and the expressions of inflammatory cytokines, transglutaminase 2 (TGM2) and ferroptosis markers were quantified. MAM formation and mitochondrial function regulated by TGM2, including mitochondrial Ca
resultsP.g-OMVs induced significant cognitive impairment and neurodegeneration in mice, evidenced by escape latency in the MWM (p < 0.001) and accumulation of amyloid β plaques and hyperphosphorylated tau. RNA-seq highlighted DEGs enriched in mitochondrial pathways, notably targeting TGM2. In vitro, P.g-OMVs triggered inflammation evidenced by increased pro-inflammatory cytokines (IL-1β, IL-17, etc.) and reduced levels of IL-10 (p < 0.05), and led to the upregulation of TGM2 (p < 0.05). Crucially, co-localization of mitochondria and ER suggested that P.g-OMVs promoted MAM formation in neurons, accompanied by aberrant mitochondrial Ca
conclusionsOur findings demonstrate that P.g-OMVs drive neuroinflammation and neuronal ferroptosis through a MAMs-associated mechanism. TGM2 acts as a key mediator, promoting MAM formation and subsequent mitochondrial dysfunction. These findings highlight TGM2 represents a potential therapeutic target for neuroinflammatory conditions linked to oral pathogens.
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