ArticleInfection and immunity2006
The K1 serotype capsular polysaccharide of Porphyromonas gingivalis elicits chemokine production from murine macrophages that facilitates cell migration.
Article in Infection and immunity, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 51 citations in OpenAlex.
- Microbial crosstalk along the oral-gut axis: organ-specific oncogenic adaptations of Porphyromonas gingivalis and Fusobacterium nucleatum.Neoplasia (New York, N.Y.) · 2026Review
- Capsular polysaccharides of Acinetobacter baumannii modulate antimicrobial resistance and innate immune response.Scientific reports · 2026Article
- Tobacco-enhanced biofilm formation by Porphyromonas gingivalis and other oral microbes.Molecular oral microbiology · 2024Review
- Review
- Porphyromonas gingivalis Virulence Factors and Clinical Significance in Periodontal Disease and Coronary Artery DiseasesPathogens (Basel, Switzerland) · 2022Review
- Characterization of a Bacterial Kinase That Phosphorylates Dihydrosphingosine to Form dhS1P.Microbiology spectrum · 2022Article
- Association betweenFrontiers in cellular and infection microbiology · 2022Review
- AFrontiers in oral health · 2021Article
- Comparative Study of Immunogenic Properties of Purified Capsular Polysaccharides fromInfection and immunity · 2020Article
- Roles of Porphyromonas gingivalis and its virulence factors in periodontitis.Advances in protein chemistry and structural biology · 2020Review
- Alzheimer's Disease-Like Pathology Triggered byFrontiers in immunology · 2020Article
- Sugar-Coated Killer: Serotype 3 Pneumococcal Disease.Frontiers in cellular and infection microbiology · 2020Review
- Immunological Pathways Triggered byMediators of inflammation · 2019Review
- Aging and contribution of MyD88 and TRIF to expression of TLR pathway-associated genes following stimulation with Porphyromonas gingivalis.Journal of periodontal research · 2015Article
- Group B Streptococcus and Streptococcus suis capsular polysaccharides induce chemokine production by dendritic cells via Toll-like receptor 2- and MyD88-dependent and -independent pathways.Infection and immunity · 2013Article
- Porphyromonas gingivalis virulence in a Drosophila melanogaster model.Infection and immunity · 2011Article
- Immune response of macrophages from young and aged mice to the oral pathogenic bacterium Porphyromonas gingivalis.Immunity & ageing : I & A · 2010Article
- The core genome of the anaerobic oral pathogenic bacterium Porphyromonas gingivalis.BMC microbiology · 2010Article
- Tobacco upregulates P. gingivalis fimbrial proteins which induce TLR2 hyposensitivity.PloS one · 2010Article
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Porphyromonas gingivalis is the principal organism associated with aggressive forms of generalized periodontal disease. Previous reports have suggested that encapsulated P. gingivalis strains are more virulent than unencapsulated strains; however, the contribution of capsular polysaccharide (CPS) to the virulence of this organism is poorly understood. Since periodontal disease presents with a complex inflammatory cell lesion comprised of neutrophils and monocytes, we cultured murine peritoneal macrophages with heat-killed P. gingivalis W83, CPS purified from P. gingivalis strain W83, and the seven known serotype-specific P. gingivalis CPS and assessed the ability of supernatant fluids produced by challenged macrophages to attract naïve inflammatory cells. We also defined JE/MCP-1, KC, MIP-2, and RANTES production in response to the P. gingivalis CPS antigens. We observed that supernatant fluids collected from macrophages incubated with P. gingivalis W83 and serotype K1 CPS stimulated the migration of naïve murine bone marrow-derived polymorphonuclear leukocytes in an in vitro cell migration chamber. CPS from W83 and the K1 serotype elicited potent chemokine secretion patterns for macrophages, while those specific to serotypes K2 to K7 were significantly less stimulatory. Reverse transcription-PCR and enzyme-linked immunosorbent assay revealed JE/MCP-1, KC, MIP-2, and RANTES expression from murine macrophages which had been challenged with purified P. gingivalis W83 CPS. Chemokine production appeared to be dependent on both the dose of and time of exposure to P. gingivalis W83 CPS. These data demonstrate that the P. gingivalis serotype K1 CPS elicits chemokine production from phagocytic cells. Furthermore, these data suggest that the host response to this antigen may contribute to the formation of the inflammatory cell lesion observed during P. gingivalis-elicited periodontal disease.
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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.