ArticleMicrobes and infection2015
Porphyromonas gingivalis attenuates ATP-mediated inflammasome activation and HMGB1 release through expression of a nucleoside-diphosphate kinase.
Article in Microbes and infection, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 63 citations in OpenAlex.
- Intraperitoneal Injection of theInternational journal of molecular sciences · 2024Article
- Dying for a cause: The pathogenic manipulation of cell death and efferocytic pathways.Molecular oral microbiology · 2024Review
- Illuminating the oral microbiome: cellular microbiology.FEMS microbiology reviews · 2023Article
- Classifying Integrated Signature Molecules in Macrophages of Rheumatoid Arthritis, Osteoarthritis, and Periodontal Disease: An Omics-Based Study.Current issues in molecular biology · 2022Article
- Inflammasome Activation in Gingival Epithelial Cells.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Bacterial subversion of NLR-mediated immune responses.Frontiers in immunology · 2022Review
- Release mechanisms of major DAMPs.Apoptosis : an international journal on programmed cell death · 2021Review
- Key Elements of Gingival Epithelial Homeostasis upon Bacterial Interaction.Journal of dental research · 2021Review
- P2RX7 at the Host-Pathogen Interface of Infectious Diseases.Microbiology and molecular biology reviews : MMBR · 2021Review
- Inflammasomes in Alveolar Bone Loss.Frontiers in immunology · 2021Review
- PANoptosis: A New Insight Into Oral Infectious Diseases.Frontiers in immunology · 2021Review
- Article
- Extracellular ATP as an Inter-Kingdom Signaling Molecule: Release Mechanisms by Bacteria and Its Implication on the Host.International journal of molecular sciences · 2020Review
- Diverse roles of nucleoside diphosphate kinase in genome stability and growth fitness.Current genetics · 2020Review
- Cytolethal distending toxin-induced release of interleukin-1β by human macrophages is dependent upon activation of glycogen synthase kinase 3β, spleen tyrosine kinase (Syk) and the noncanonical inflammasome.Cellular microbiology · 2020Article
- Article
- Immunological Pathways Triggered byMediators of inflammation · 2019Review
- The role ofInfectious agents and cancer · 2019Review
- Oral Mucosal Epithelial Cells.Frontiers in immunology · 2019Review
- Porphyromonas gingivalis traffics into endoplasmic reticulum-rich-autophagosomes for successful survival in human gingival epithelial cells.Virulence · 2018Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Many intracellular pathogens evade the innate immune response in order to survive and proliferate within infected cells. We show that Porphyromonas gingivalis, an intracellular opportunistic pathogen, uses a nucleoside-diphosphate kinase (NDK) homolog to inhibit innate immune responses due to stimulation by extracellular ATP, which acts as a danger signal that binds to P2X7 receptors and induces activation of an inflammasome and caspase-1. Thus, infection of gingival epithelial cells (GECs) with wild-type P. gingivalis results in inhibition of ATP-induced caspase-1 activation. However, ndk-deficient P. gingivalis is less effective than wild-type P. gingivalis in reducing ATP-mediated caspase-1 activation and secretion of the pro-inflammatory cytokine, IL-1β, from infected GECs. Furthermore, P. gingivalis NDK modulates release of high-mobility group protein B1 (HMGB1), a pro-inflammatory danger signal, which remains associated with chromatin in healthy cells. Unexpectedly, infection with either wild-type or ndk-deficient P. gingivalis causes release of HMGB1 from the nucleus to the cytosol. But HMGB1 is released to the extracellular space when uninfected GECs are further stimulated with ATP, and there is more HMGB1 released from the cells when ATP-treated cells are infected with ndk-deficient mutant than wild-type P. gingivalis. Our results reveal that NDK plays a significant role in inhibiting P2X7-dependent inflammasome activation and HMGB1 release from infected GECs.
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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.