ArticleMolecular oral microbiology2013
Mechanism and implications of CXCR4-mediated integrin activation by Porphyromonas gingivalis.
Article in Molecular oral microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
28 citing papers in PubMed, 36 citations in OpenAlex.
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- Innovative strategies targeting oral microbial dysbiosis: unraveling mechanisms and advancing therapies for periodontitis.Frontiers in cellular and infection microbiology · 2025Review
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- CD47 and thrombospondin-1 contribute to immune evasion byProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Periodontal pathogens and cancer development.Periodontology 2000 · 2024Review
- The potential crosstalk genes and molecular mechanisms between glioblastoma and periodontitis.Scientific reports · 2024Article
- Porphyromonas gingivalis induction of TLR2 association with Vinculin enables PI3K activation and immune evasion.PLoS pathogens · 2023Article
- Sialidase facilitatesFrontiers in cellular and infection microbiology · 2023Article
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- Acute and Chronic Pain from Facial Skin and Oral Mucosa: Unique Neurobiology and Challenging Treatment.International journal of molecular sciences · 2021Review
- Crosstalk between Venous Thromboembolism and Periodontal Diseases: A Bioinformatics Analysis.Disease markers · 2021Article
- Oral PathogenMicroorganisms · 2020Article
- Infectious Triggers in Periodontitis and the Gut in Rheumatoid Arthritis (RA): A Complex Story About Association and Causality.Frontiers in immunology · 2020Review
- Roles of Porphyromonas gingivalis and its virulence factors in periodontitis.Advances in protein chemistry and structural biology · 2020Review
- Pathogenesis of Important Virulence Factors ofFrontiers in cellular and infection microbiology · 2019Review
- Characterization and development of SAPP as a specific peptidic inhibitor that targets Porphyromonas gingivalis.Molecular oral microbiology · 2018Article
- Impaired innate immune signaling due to combined Toll-like receptor 2 and 4 deficiency affects both periodontitis and atherosclerosis in response to polybacterial infection.Pathogens and disease · 2018Article
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 2 countries.
Funding
Abstract
In monocytes and macrophages, the interaction of Porphyromonas gingivalis with Toll-like receptor 2 (TLR2) leads to the activation of a MyD88-dependent antimicrobial pathway and a phosphatidylinositol-3 kinase (PI3K) -dependent pro-adhesive pathway, which activates the β2 -integrin complement receptor 3 (CR3). By means of its fimbriae, P. gingivalis binds CXC-chemokine receptor 4 (CXCR4) and induces crosstalk with TLR2 that inhibits the MyD88-dependent antimicrobial pathway. In this paper, we investigated the impact of the P. gingivalis-CXCR4 interaction on the pro-adhesive pathway. Using human monocytes, mouse macrophages, or receptor-transfected cell lines, we showed that the binding of P. gingivalis fimbriae to CXCR4 induces CR3 activation via PI3K, albeit in a TLR2-independent manner. An isogenic strain of P. gingivalis expressing mutant fimbriae that do not interact with CXCR4 failed to efficiently activate CR3, leading to enhanced susceptibility to killing in vivo compared with the wild-type organism. This in vivo observation is consistent with previous findings that activated CR3 mediates safe entry of P. gingivalis into macrophages. Taken together with our previous work, these results indicate that the interaction of P. gingivalis with CXCR4 leads to inhibition of antimicrobial responses and enhancement of pro-adhesive responses, thereby maximizing its adaptive fitness in the mammalian host.
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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.