ArticlePloS one2017
Mechanisms by which Porphyromonas gingivalis evades innate immunity.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Polymicrobial-driven NLRP6 inflammasome regulates IL-1β production and alveolar bone loss in a murine model of periodontitis.PLoS pathogens · 2026Article
- Periodontal Disease and Its Association withMicroorganisms · 2026Review
- Effects ofMicroorganisms · 2025Article
- Probiotics and amelioration of periodontitis: significant roles ofFrontiers in microbiology · 2025Article
- Role of bestatin as a treatment for periodontitis.Frontiers in dental medicine · 2025Review
- Linking Periodontitis with Inflammatory Bowel Disease through the Oral-Gut Axis: The Potential Role ofBiomedicines · 2024Review
- Arginine-specific gingipains (RgpA/RgpB) knockdown modulates neutrophil machinery.Journal of oral microbiology · 2024Article
- Multispecies biofilm behavior and host interaction support the association of Tannerella serpentiformis with periodontal health.Molecular oral microbiology · 2023Article
- Elucidating Cellular Metabolism and Protein Difference Data from DIGE Proteomics Experiments Using Enzyme Assays.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Insight into the Relationship between Oral Microbiota and the Inflammatory Bowel Disease.Microorganisms · 2022Review
- Enhanced Responsive Formation of Extracellular Traps in Macrophages Previously Exposed to Porphyromonas gingivalis.Inflammation · 2022Article
- Links between Insulin Resistance and Periodontal Bacteria: Insights on Molecular Players and Therapeutic Potential of Polyphenols.Biomolecules · 2022Review
- Article
- New Insights into the Role of Oral Microbiota Dysbiosis in the Pathogenesis of Inflammatory Bowel Disease.Digestive diseases and sciences · 2022Review
- Sphingolipid-Containing Outer Membrane Vesicles Serve as a Delivery Vehicle To Limit Macrophage Immune Response to Porphyromonas gingivalis.Infection and immunity · 2021Article
- Microbial Lipid A Remodeling Controls Cross-Presentation Efficiency and CD8 T Cell Priming by Modulating Dendritic Cell Function.Infection and immunity · 2021Article
- Possible Immunotherapeutic Strategies Based on Carcinogen-Dependent Subgroup Classification for Oral Cancer.Frontiers in molecular biosciences · 2021Review
- Review
- Polymicrobial synergy within oral biofilm promotes invasion of dendritic cells and survival of consortia members.NPJ biofilms and microbiomes · 2019Article
- Pathogenesis of Important Virulence Factors ofFrontiers in cellular and infection microbiology · 2019Review
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
The oral cavity is home to unique resident microbial communities whose interactions with host immunity are less frequently studied than those of the intestinal microbiome. We examined the stimulatory capacity and the interactions of two oral bacteria, Porphyromonas gingivalis (P. gingivalis) and Fusobacterium nucleatum (F. nucleatum), on Dendritic Cell (DC) activation, comparing them to the effects of the well-studied intestinal microbe Escherichia coli (E. coli). Unlike F. nucleatum and E. coli, P. gingivalis failed to activate DCs, and in fact silenced DC responses induced by F. nucleatum or E. coli. We identified a variant strain of P. gingivalis (W50) that lacked this immunomodulatory activity. Using biochemical approaches and whole genome sequencing to compare the two substrains, we found a point mutation in the hagA gene. This protein is though to be involved in the alteration of the PorSS/gingipain pathway, which regulates protein secretion into the extracellular environment. A proteomic comparison of the secreted products of the two substrains revealed enzymatic differences corresponding to this phenotype. We found that P. gingivalis secretes gingipain(s) that inactivate several key proinflammatory mediators made by DCs and/or T cells, but spare Interleukin-1 (IL-1) and GM-CSF, which can cause capillary leaks that serve as a source of the heme that P. gingivalis requires for its survival, and GM-CSF, which can cause epithelial-cell growth. Taken together, our results suggest that P. gingivalis has evolved potent mechanisms to modulate its virulence factors and dampen the innate immune response by selectively inactivating most proinflammatory cytokines.
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