ArticleInfection and immunity2002
Discrete proteolysis of focal contact and adherens junction components in Porphyromonas gingivalis-infected oral keratinocytes: a strategy for cell adhesion and migration disabling.
Article in Infection and immunity, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.
- Pooled it
- Article
- P. gingivalis-host interactions direct antibiotic adjuvants for periodontitis antimicrobial therapy.International journal of oral science · 2026Article
- Oral Microbiome Dynamics in Patients with Acute Lymphoblastic Leukemia and Oral Mucositis.Microorganisms · 2026Article
- Natural and induced immune responses in oral cavity and saliva.BMC immunology · 2025Review
- Cell Junctions in Periodontal Health and Disease: An Insight.European journal of dentistry · 2024Article
- Critical roles of adherens junctions in diseases of the oral mucosa.Tissue barriers · 2023Article
- [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- Human Oral Keratinocytes Challenged byInternational journal of microbiology · 2022Article
- Oral Mucosal Epithelial Cells.Frontiers in immunology · 2019Review
- Porphyromonas gingivalis bypasses epithelial barrier and modulates fibroblastic inflammatory response in an in vitro 3D spheroid model.Scientific reports · 2018Article
- Genetic, Transcriptome, Proteomic, and Epidemiological Evidence for Blood-Brain Barrier Disruption and Polymicrobial Brain Invasion as Determinant Factors in Alzheimer's Disease.Journal of Alzheimer's disease reports · 2017Article
- Interferon Regulatory Factor 6 Promotes Keratinocyte Differentiation in Response to Porphyromonas gingivalis.Infection and immunity · 2017Article
- TheFrontiers in aging neuroscience · 2017Article
- Periodontitis, Microbiomes and their Role in Alzheimer's Disease.Frontiers in aging neuroscience · 2017Article
- Microbial Degradation of Cellular Kinases Impairs Innate Immune Signaling and Paracrine TNFα Responses.Scientific reports · 2016Article
- The impact of virulence factors of Porphyromonas gingivalis on wound healing in vitro.Journal of oral microbiology · 2015Article
- The influence of oral bacteria on epithelial cell migration in vitro.Mediators of inflammation · 2013Article
- Interaction of oral bacteria with gingival epithelial cell multilayers.Molecular oral microbiology · 2011Article
- Role of Porphyromonas gingivalis phosphoserine phosphatase enzyme SerB in inflammation, immune response, and induction of alveolar bone resorption in rats.Infection and immunity · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Adhesive interactions of cells are critical to tissue integrity. We show that infection with Porphyromonas gingivalis, a major pathogen in the periodontal disease periodontitis, interferes with both cell-matrix and cell-cell adhesion in the oral keratinocyte cell line HOK-16. Thus, infected cells showed reduced adhesion to extracellular matrix, changes in morphology from spread to rounded, and impaired motility on purified matrices in Transwell migration assays and scratch assays. Western blot analysis of P. gingivalis-challenged HOK-16 cells revealed proteolysis of focal contact components (e.g., focal adhesion kinase), adherens junction proteins (e.g., catenins), and adhesion signaling molecules (e.g., the tyrosine kinase SRC). Proteolysis was selective, since important components of adherens junctions (E-cadherin) or signaling molecules (extracellular signal-regulated kinases ERK1/2) were not degraded. The virulence factors gingipains, cysteine proteinases expressed by P. gingivalis, are likely responsible for this proteolytic attack, since they directly digested specific proteins in pull-down experiments, and their proteolytic activity was blocked by the cysteine proteinase inhibitor N-alpha-p-tosyl-L-lysine chloromethyl ketone and also by a caspase inhibitor. Proteolysis was strain dependent, such that ATCC 33277 and 381 had high proteolytic potential, whereas W50 showed almost no proteolytic activity. These findings may help explain the formation of gingival pockets between cementum and periodontal epithelium, a hallmark of periodontitis. Furthermore, they illustrate a new pathogenetic paradigm of infection whereby bacteria may disrupt the integrity of epithelia.
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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.