ArticlePLoS pathogens2019
Porphyromonas gingivalis induces penetration of lipopolysaccharide and peptidoglycan through the gingival epithelium via degradation of junctional adhesion molecule 1.
Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed.
- Article
- Heated tobacco product-derived aerosol extract impairs gingival epithelial barrier function via CXADR downregulation.Toxicology reports · 2026Article
- Antioxidant, Antibacterial, and Antivirulence Activities of a Bioactive Fraction fromAntioxidants (Basel, Switzerland) · 2026Article
- Effect of gut bacterial extracellular vesicles on angiogenic potential and vascular integrity: positive and negative aspects.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Neonicotinoid pesticides disrupt gingival epithelial barrier function.Toxicology reports · 2026Article
- Tobacco-Induced Oral Dysbiosis and Microbial Shifts: A Narrative Review of Their Role in Systemic Inflammation and Disease.Microorganisms · 2026Review
- Review
- Live tissue microbiota and bacterial translocation: mechanisms and translational perspectives in cardiometabolic diseases.Reviews in endocrine & metabolic disorders · 2026Review
- VPS13B, gene responsible for Cohen syndrome, regulates gingival epithelial barrier function via intracellular trafficking of coxsackievirus and adenovirus receptor.Scientific reports · 2026Article
- Dihydromyricetin exhibits potent antibacterial activity and virulence factor inhibitory effects againstFrontiers in oral health · 2026Article
- The oral-lung axis in lung cancer: microbial translocation, immune reprogramming, and clinical implications.Frontiers in immunology · 2026Review
- Synergistic Roles of Fimbriae and Gingipain Genotypes inInternational journal of dentistry · 2026Article
- Periodontitis salivary microbiota exacerbates colitis by CXCL3 derived from gut microbiota-induced macrophages.Microbiome · 2025Article
- Impact of Periodontal Host-Modulation Therapies on Oral-Gut Microbiome Axis in Periodontitis Patients with Hematological Diseases: A Narrative Review.Life (Basel, Switzerland) · 2025Review
- Identification of Bacterial Networks and Relationship to Host Responses in Early Periodontitis Population over 24 Months.International journal of molecular sciences · 2025Article
- Microbial Coaggregation in the Oral Cavity: Molecular Interactions and Current Insights.International journal of molecular sciences · 2025Review
- Advancements in understanding tumor-resident bacteria and their application in cancer therapy.Military Medical Research · 2025Review
- Gingipain regulates isoform switches of PD-L1 in macrophages infected with Porphyromonas gingivalis.Scientific reports · 2025Article
- The efficacy of antimicrobial therapies in the treatment of mixed biofilms formed between Candida albicans and Porphyromonas gingivalis during epithelial cell infection in the aspiration pneumonia model.Medical microbiology and immunology · 2025Article
- Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Porphyromonas gingivalis is a major pathogen in severe and chronic manifestations of periodontal disease, which is one of the most common infections of humans. A central feature of P. gingivalis pathogenicity is dysregulation of innate immunity at the gingival epithelial interface; however, the molecular basis underlying P. gingivalis-dependent abrogation of epithelial barrier function remains unknown. Gingival epithelial cells express junctional adhesion molecule (JAM1), a tight junction-associated protein, and JAM1 homodimers regulate epithelial barrier function. Here we show that Arg-specific or Lys-specific cysteine proteases (gingipains) secreted by P. gingivalis can specifically degrade JAM1 at K134 and R234 in gingival epithelial cells, resulting in permeability of the gingival epithelium to 40 kDa dextran, lipopolysaccharide (LPS), and proteoglycan (PGN). A P. gingivalis strain lacking gingipains was impaired in degradation of JAM1. Knockdown of JAM1 in monolayer cells and a three-dimensional multilayered tissue model also increased permeability to LPS, PGN, and gingipains. Inversely, overexpression of JAM1 in epithelial cells prevented penetration by these agents following P. gingivalis infection. Our findings strongly suggest that P. gingivalis gingipains disrupt barrier function of stratified squamous epithelium via degradation of JAM1, allowing bacterial virulence factors to penetrate into subepithelial tissues.
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