ArticleInfection and immunity2001
Porphyromonas gingivalis gingipain-R enhances interleukin-8 but decreases gamma interferon-inducible protein 10 production by human gingival fibroblasts in response to T-cell contact.
Article in Infection and immunity, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Association between Periodontal Disease and Cognitive Impairment in Adults.International journal of environmental research and public health · 2023Pooled it
- Impact of commercial gut health interventions on caecal metagenome and broiler performance.Microbiome · 2025Article
- Periodontal pathogens and cancer development.Periodontology 2000 · 2024Review
- Oral microbiota-host interaction: the chief culprit of alveolar bone resorption.Frontiers in immunology · 2024Review
- Mesenchymal Stromal Cells from Healthy and Inflamed Human Gingiva Respond Differently toInternational journal of molecular sciences · 2022Article
- Shut-Down of Type IX Protein Secretion Alters the Host Immune Response toFrontiers in cellular and infection microbiology · 2022Article
- Effect of scaling on the invasion of oral microorganisms into dentinal tubules including the response of pulpal cells-an in vitro study.Clinical oral investigations · 2021Article
- Targeting a cysteine protease from a pathobiont alleviates experimental arthritis.Arthritis research & therapy · 2020Article
- Article
- Vaccination with recombinant RgpA peptide protects against Porphyromonas gingivalis-induced bone loss.Journal of periodontal research · 2017Article
- Suppression of T-cell chemokines by Porphyromonas gingivalis.Infection and immunity · 2013Article
- Enteric bacterial proteases in inflammatory bowel disease- pathophysiology and clinical implications.World journal of gastroenterology · 2013Review
- Luteolin and fisetin inhibit the effects of lipopolysaccharide obtained from Porphyromonas gingivalis in human gingival fibroblasts.Molecular biology reports · 2013Article
- Cleavage of protease-activated receptors on an immortalized oral epithelial cell line by Porphyromonas gingivalis gingipains.Microbiology (Reading, England) · 2009Article
- Expression and regulation of the NALP3 inflammasome complex in periodontal diseases.Clinical and experimental immunology · 2009Article
- The RgpA-Kgp proteinase-adhesin complexes of Porphyromonas gingivalis Inactivate the Th2 cytokines interleukin-4 and interleukin-5.Infection and immunity · 2009Article
- Corruption of innate immunity by bacterial proteases.Journal of innate immunity · 2009Review
- Arginine-specific gingipains from Porphyromonas gingivalis deprive protective functions of secretory leucocyte protease inhibitor in periodontal tissue.Clinical and experimental immunology · 2006Article
- A functional virulence complex composed of gingipains, adhesins, and lipopolysaccharide shows high affinity to host cells and matrix proteins and escapes recognition by host immune systems.Infection and immunity · 2005Article
- Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proteases produced by Porphyromonas gingivalis, an oral pathogen, are considered important virulence factors and may affect the responses of cells equipped with proteinase-activated receptors. The aim of this study was to investigate the effect of the arginine-specific cysteine protease gingipain-R produced by P. gingivalis on chemokine production by human gingival fibroblasts (HGF) and the effect of gingipain-R treatment on the subsequent contact-dependent activation of HGF by T cells. HGF incubated in the presence of purified 47-kDa gingipain-R showed increased levels of interleukin-8 (IL-8) mRNA. Cyclooxygenase-2 (COX-2) mRNA was also induced. Further exposure of HGF to activated T cells resulted in the dose- and time-dependent enhancement of IL-8 transcription and release. T-cell membrane-bound tumor necrosis factor (TNF) was the ligand inducing IL-8 production by HGF, since TNF neutralization abrogated HGF responses to T-cell contact. The enhanced IL-8 release was due, at least in part, to prostaglandin-E(2) production, which was mostly blocked by indomethacin. Gingipain-R proteolytic activity was required since heat inactivation, specific synthetic protease inhibitors, and the natural substrate competitor histatin 5 abrogated its effects. The enhanced production of IL-8 in response to T-cell contact was specific since monocyte chemotactic protein-1 (MCP-1) production was unaffected while interferon-gamma-inducible protein-10 (IP-10) was inhibited. The sum of these activities may result in the recruitment of differential cell types to sites of inflammation since IL-8 preferentially recruits neutrophils and IP-10 attracts activated T cells and may be relevant to the pathogenesis of periodontitis.
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