ArticleInfection and immunity2009
Entry of Porphyromonas gingivalis outer membrane vesicles into epithelial cells causes cellular functional impairment.
Article in Infection and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 1 of them a synthesis that pooled it.
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Who cites it
86 citing papers in PubMed, 1 synthesis or guideline pooled it, 149 citations in OpenAlex.
- Systematic Review: Porphyromonas gingivalis Outer Membrane Vesicles From Pathogenesis to Therapeutic Implications.International dental journal · 2026Pooled it
- Article
- Porphyromonas gingivalis Outer Membrane Vesicles-Associated DNA Triggers Inflammation by Inducing IL-6 in Astrocytes.Molecular oral microbiology · 2026Article
- The Antimicrobial Efficacy of New Antibiotic Combinations against Bacteria Associated with Endo-perio Lesions in Deciduous Teeth: AnInternational journal of clinical pediatric dentistry · 2026Article
- The Role of Oral Pathobionts' Outer Membrane Vesicles in Cancer Pathology and Therapeutic Development.Cells · 2026Review
- Review
- Comparative characterization reveals conserved and divergent ecological traits of oral corynebacteria.Microbiology spectrum · 2026Article
- Oral Dysbiosis and Neuroinflammation: Implications for Alzheimer's, Parkinson's and Mood Disorders.Microorganisms · 2026Review
- Crosstalk between iron metabolism dysregulation and the oral microbiome in periodontitis.Journal of oral microbiology · 2026Review
- The oral-vascular axis: immune mechanisms linking periodontal dysbiosis to systemic vascular pathology.Frontiers in immunology · 2026Review
- Microbial Coaggregation in the Oral Cavity: Molecular Interactions and Current Insights.International journal of molecular sciences · 2025Review
- Extracellular Vesicles fromMicroorganisms · 2025Article
- Bacterial Extracellular Vesicles: An Emerging Concern in the Field of Environmental Contamination-Characterization, Impacts, and Response Strategies.Microorganisms · 2025Review
- Porphyromonas gingivalis Type 9 Secretion System Promotes Dysregulation of Vascular Smooth Muscle Cell Plasticity With Perturbed TGF-β/Smad Signaling.MicrobiologyOpen · 2025Article
- The Periodontal-Cardiovascular Disease Association: Molecular Mechanisms and Clinical Implications.International journal of molecular sciences · 2025Review
- Alzheimer's Disease andLife (Basel, Switzerland) · 2025Review
- Outer membrane vesicles ofFrontiers in microbiology · 2025Review
- Emerging role of gut microbiota extracellular vesicle in neurodegenerative disorders and insights on their therapeutic management.iMetaOmics · 2024Review
- Outer Membrane Vesicles Derived From Fusobacterium nucleatum Trigger Periodontitis Through Host Overimmunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Oral Pathobiont-Derived Outer Membrane Vesicles in the Oral-Gut Axis.International journal of molecular sciences · 2024Review
26 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Porphyromonas gingivalis, a periodontal pathogen, secretes outer membrane vesicles (MVs) that contain major virulence factors, including proteases termed gingipains (Arg-gingipain [Rgp] and Lys-gingipain [Kgp]). We recently showed that P. gingivalis MVs swiftly enter host epithelial cells via an endocytosis pathway and are finally sorted to lytic compartments. However, it remains unknown whether MV entry impairs cellular function. Herein, we analyzed cellular functional impairment following entry of P. gingivalis into epithelial cells, including HeLa and immortalized human gingival epithelial (IHGE) cells. After being taken up by endocytic vacuoles, MVs degraded the cellular transferrin receptor (TfR) and integrin-related signaling molecules, such as paxillin and focal adhesion kinase (FAK), which resulted in depletion of intracellular transferrin and inhibition of cellular migration. Few Rgp-null MVs entered the cells, and these negligibly degraded TfR, whereas paxillin and FAK degradation was significant. In contrast, Kgp-null MVs clearly entered the cells and degraded TfR, while they scarcely degraded paxillin and FAK. In addition, both wild-type and Kgp-null MVs significantly impaired cellular migration, whereas the effect of Rgp-null MVs was limited. Our findings suggest that, following entry of P. gingivalis MVs into host cells, MV-associated gingipains degrade cellular functional molecules such as TfR and paxillin/FAK, resulting in cellular impairment, indicating that P. gingivalis MVs are potent vehicles for transmission of virulence factors into host cells and are involved in the etiology of periodontitis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.