ArticlePloS one2015
Cleavage of host cytokeratin-6 by lysine-specific gingipain induces gingival inflammation in periodontitis patients.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- Interspecies regulation of virulence through gingipain inhibition by a Tannerella forsythia serpin.EMBO reports · 2026Article
- Advanced immunodiagnostics for periodontal disease: Targeted detection of Kgp and RgpB using A7 and G1 antibody set.Journal of advanced research · 2026Article
- Bidirectional relationship between the biofilm ofMicrobiology spectrum · 2026Article
- Gingipains disrupt bone homeostasis via dual regulation of osteogenesis and osteoclastogenesis through exosomal miR-146a-5p/TRAF6 signaling.Frontiers in cellular and infection microbiology · 2025Article
- Association between serum neurofilament light chain and periodontitis.Clinical oral investigations · 2024Article
- Variability in Genomic and Virulent Properties ofFrontiers in cellular and infection microbiology · 2019Article
- Antioxidant and Anti-Inflammatory Properties of Anthocyanins Extracted fromOxidative medicine and cellular longevity · 2019Article
- Article
- Gingipain of Porphyromonas gingivalis manipulates M1 macrophage polarization through C5a pathway.In vitro cellular & developmental biology. Animal · 2017Article
- Porphyromonas gingivalis gingipains cause defective macrophage migration towards apoptotic cells and inhibit phagocytosis of primary apoptotic neutrophils.Cell death & disease · 2017Article
- HMGB1 Promotes Intraoral Palatal Wound Healing through RAGE-Dependent Mechanisms.International journal of molecular sciences · 2016Article
- Review
- PKCδ inhibition normalizes the wound-healing capacity of diabetic human fibroblasts.The Journal of clinical investigation · 2016Article
- Porphyromonas gingivalis-induced miR-132 regulates TNFα expression in THP-1 derived macrophages.SpringerPlus · 2016Article
- Inhibitors of bacterial protease enzymes for periodontal therapy.Clinical and experimental dental research · 2015Article
- Noncanonical activation of β-catenin by Porphyromonas gingivalis.Infection and immunity · 2015Article
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background/purposeLysine-specific gingipain (Kgp) is a virulence factor secreted from Porphyromonas gingivalis (P. gingivalis), a major etiological bacterium of periodontal disease. Keratin intermediate filaments maintain the structural integrity of gingival epithelial cells, but are targeted by Kgp to produce a novel cytokeratin 6 fragment (K6F). We investigated the release of K6F and its induction of cytokine secretion.
methodsK6F present in the gingival crevicular fluid of periodontal disease patients and in gingipain-treated rat gingival epithelial cell culture supernatants was measured by matrix-assisted laser desorption/ionization time-of-flight mass spectrometer-based rapid quantitative peptide analysis using BLOTCHIP. K6F in gingival tissues was immunostained, and cytokeratin 6 protein was analyzed by immunofluorescence staining and flow cytometry. Activation of MAPK in gingival epithelial cells was evaluated by immunoblotting. ELISA was used to measure K6F and the cytokines release induced by K6F. Human gingival fibroblast migration was assessed using a Matrigel invasion chamber assay.
resultsWe identified K6F, corresponding to the C-terminus region of human cytokeratin 6 (amino acids 359-378), in the gingival crevicular fluid of periodontal disease patients and in the supernatant from gingival epithelial cells cultured with Kgp. K6F antigen was distributed from the basal to the spinous epithelial layers in gingivae from periodontal disease patients. Cytokeratin 6 on gingival epithelial cells was degraded by Kgp, but not by Arg-gingipain, P. gingivalis lipopolysaccharide or Actinobacillus actinomycetemcomitans lipopolysaccharide. K6F, but not a scrambled K6F peptide, induced human gingival fibroblast migration and secretion of interleukin (IL)-6, IL-8 and monocyte chemoattractant protein-1. These effects of K6F were mediated by activation of p38 MAPK and Jun N-terminal kinase, but not p42/44 MAPK or p-Akt.
conclusionKgp degrades gingival epithelial cell cytokeratin 6 to K6F that, on release, induces invasion and cytokine secretion by human gingival fibroblasts. Thus, Kgp may contribute to the development of periodontal disease.
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