ArticleBMC microbiology2013
Porphyromonas gingivalis downregulates the immune response of fibroblasts.
Article in BMC microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 66 citations in OpenAlex.
- Precise assessment of facial skin based on multimodal data fusion of the microbiome.Quantitative biology (Beijing, China) · 2026Article
- Therapeutic potency and the related mechanism of deinoxanthin in experimental animal and cell models of periodontitis.Scientific reports · 2026Article
- Immunomodulatory effects of eubiotic and dysbiotic multi-species biofilms on oral keratinocytes.BMC oral health · 2025Article
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- Porphyromonas gingivalis outer membrane vesicles alter cortical neurons and Tau phosphorylation in the embryonic mouse brain.PloS one · 2025Article
- Synergistic effects ofFrontiers in cellular and infection microbiology · 2025Article
- The Role of Gingival Fibroblasts in the Pathogenesis of Periodontitis.Journal of dental research · 2023Review
- IL-1β and TNF-α play an important role in modulating the risk of periodontitis and Alzheimer's disease.Journal of neuroinflammation · 2023Article
- Local and Systemic Effects ofMicroorganisms · 2023Review
- Oral microbiome mediated inflammation, a potential inductor of vascular diseases: a comprehensive review.Frontiers in cardiovascular medicine · 2023Review
- Pathogenesis of periodontitis - A potential role for epithelial-mesenchymal transition.The Japanese dental science review · 2022Review
- Article
- Different expression patterns of inflammatory cytokines induced by lipopolysaccharides from Escherichia coli or Porphyromonas gingivalis in human dental pulp stem cells.BMC oral health · 2022Article
- Article
- Chlorogenic Acid as a Positive Regulator in LPS-PG-Induced Inflammation via TLR4/MyD88-Mediated NF-Mediators of inflammation · 2022Article
- Antimicrobial and anti-inflammatory activity of Cystatin C on human gingival fibroblast incubated withPeerJ · 2022Article
- Dysbiosis of the duodenal microbiota as a diagnostic marker for pancreaticobiliary cancer.World journal of gastrointestinal oncology · 2021Article
- Natural Sulfurs Inhibit LPS-Induced Inflammatory Responses through NF-κB Signaling in CCD-986Sk Skin Fibroblasts.Life (Basel, Switzerland) · 2021Article
- Periodontal Disease and Senescent Cells: New Players for an Old Oral Health Problem?International journal of molecular sciences · 2020Review
- Activation of Gingival Fibroblasts by Bacterial Cyclic Dinucleotides and Lipopolysaccharide.Pathogens (Basel, Switzerland) · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPorphyromonas gingivalis is a key pathogen in periodontitis, an inflammatory disease leading to destruction of bone and tooth-supporting tissue. P. gingivalis possesses a number of pathogenic properties to enhance growth and survival, including proteolytic gingipains. Accumulating data shows that gingipains are involved in the regulation of host inflammatory responses. The aim of this study was to determine if P. gingivalis infection modulates the inflammatory response of fibroblasts, including the release of chemokines and cytokines. Human gingival fibroblasts or primary dermal fibroblasts were pre-stimulated with tumor-necrosis factor-α (TNF- α) and cocultured with P. gingivalis. Gingipain inhibitors were used to explore the effect of gingipains. CXCL8 levels were determined with ELISA and the relative levels of various inflammatory mediators were determined by a cytokine assay.
resultsTNF-α-triggered CXCL8 levels were completely abolished by viable P. gingivalis, whereas heat-killed P. gingivalis did not suppress CXCL8. Accumulation of CXCL8 was partially restored by an arginine-gingipain inhibitor. Furthermore, fibroblasts produced several inflammatory mediators, notably chemokines, all of which were suppressed by viable P. gingivalis.
conclusionThese findings provide evidence that fibroblast-derived inflammatory signals are modulated by heat-instable gingipains, whereby the bacteria can escape killing by the host immune system and promote its own growth and establishment. In addition, we show that fibroblasts are important mediators of inflammation in response to infection and thereby play a crucial role in determining the nature and magnitude of the invasion of immune cells.
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