ArticlePloS one2013
Treponema denticola major outer sheath protein impairs the cellular phosphoinositide balance that regulates neutrophil chemotaxis.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 19 citations in OpenAlex.
- Periodontitis and Chronic Liver Disease: Mechanistic Insights Focusing onMicroorganisms · 2026Review
- Topology and functional characterization of major outer membrane proteins of Treponema maltophilum and Treponema lecithinolyticum.Molecular oral microbiology · 2025Article
- Treponema denticola major surface protein (Msp): a key player in periodontal pathogenicity and immune evasion.Archives of microbiology · 2025Review
- Emerging oralFrontiers in oral health · 2025Article
- Periodontal Pathogens' strategies disarm neutrophils to promote dysregulated inflammation.Molecular oral microbiology · 2021Review
- Interactions Between Neutrophils and Periodontal Pathogens in Late-Onset Periodontitis.Frontiers in cellular and infection microbiology · 2021Review
- Monitoring Phosphoinositide Fluxes and Effectors During Leukocyte Chemotaxis and Phagocytosis.Frontiers in cell and developmental biology · 2021Review
- Innate Phagocyte Polarization in the Oral Cavity.Frontiers in immunology · 2021Review
- Treponema denticola stimulates Oncostatin M cytokine release and de novo synthesis in neutrophils and macrophages.Journal of leukocyte biology · 2020Article
- The Msp Protein of Treponema denticola Interrupts Activity of Phosphoinositide Processing in Neutrophils.Infection and immunity · 2019Article
- The major outer sheath protein forms distinct conformers and multimeric complexes in the outer membrane and periplasm of Treponema denticola.Scientific reports · 2017Article
- The C-terminal region of the major outer sheath protein of Treponema denticola inhibits neutrophil chemotaxis.Molecular oral microbiology · 2017Article
- Filifactor alocis Promotes Neutrophil Degranulation and Chemotactic Activity.Infection and immunity · 2016Article
- Treponema denticola upregulates MMP-2 activation in periodontal ligament cells: interplay between epigenetics and periodontal infection.Archives of oral biology · 2014Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
Abstract
The major outer sheath protein (Msp) of Treponema denticola inhibits neutrophil polarization and directed chemotaxis together with actin dynamics in vitro in response to the chemoattractant N-formyl-methionine-leucine-phenylanine (fMLP). Msp disorients chemotaxis through inhibition of a Rac1-dependent signaling pathway, but the upstream mechanisms are unknown. We challenged murine bone marrow neutrophils with enriched native Msp to determine the role of phospholipid modifying enzymes in chemotaxis and actin assembly downstream of fMLP-stimulation. Msp modulated cellular phosphoinositide levels through inhibition of phosphatidylinositol 3-kinase (PI3-kinase) together with activation of the lipid phosphatase, phosphatase and tensin homolog deleted on chromosome 10 (PTEN). Impaired phosphatidylinositol[(3,4,5)]-triphosphate (PIP3) levels prevented recruitment and activation of the downstream mediator Akt. Release of the actin capping proteins gelsolin and CapZ in response to fMLP was also inhibited by Msp exposure. Chemical inhibition of PTEN restored PIP3 signaling, as measured by Akt activation, Rac1 activation, actin uncapping, neutrophil polarization and chemotaxis in response to fMLP-stimulation, even in the presence of Msp. Transduction with active Rac1 also restored fMLP-mediated actin uncapping, suggesting that Msp acts at the level of PIP3 in the hierarchical feedback loop of PIP3 and Rac1 activation. Taken together, Msp alters the phosphoinositide balance in neutrophils, impairing the cell "compass", which leads to inhibition of downstream chemotactic events.
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Registered trials
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.