ArticleInfection and immunity2005
Inactivation of membrane tumor necrosis factor alpha by gingipains from Porphyromonas gingivalis.
Article in Infection and immunity, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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, 59 citations in OpenAlex.
- Review
- Article
- Arginine-specific gingipains (RgpA/RgpB) knockdown modulates neutrophil machinery.Journal of oral microbiology · 2024Article
- Local and Systemic Effects ofMicroorganisms · 2023Review
- Express Diagnostics of Proteolytic Activity of Periodontopathogens-Methodological Approach.Dentistry journal · 2022Article
- Proteolysis of Gingival Keratinocyte Cell Surface Proteins by Gingipains Secreted FromFrontiers in microbiology · 2020Article
- Manipulation of Neutrophils byFrontiers in cellular and infection microbiology · 2017Review
- Gingipains: Critical Factors in the Development of Aspiration Pneumonia Caused by Porphyromonas gingivalis.Journal of innate immunity · 2016Article
- Porphyromonas gingivalis gingipains selectively reduce CD14 expression, leading to macrophage hyporesponsiveness to bacterial infection.Journal of innate immunity · 2015Article
- Cleavage of host cytokeratin-6 by lysine-specific gingipain induces gingival inflammation in periodontitis patients.PloS one · 2015Article
- A pathogenic trace of Tannerella forsythia - shedding of soluble fully active tumor necrosis factor α from the macrophage surface by karilysin.Molecular oral microbiology · 2014Article
- Neutrophils alter epithelial response to Porphyromonas gingivalis in a gingival crevice model.Molecular oral microbiology · 2013Article
- The K1K2 region of Lys-gingipain of Porphyromonas gingivalis blocks induction of HLA expression by gamma interferon.Infection and immunity · 2012Article
- Pathogen-mediated proteolysis of the cell death regulator RIPK1 and the host defense modulator RIPK2 in human aortic endothelial cells.PLoS pathogens · 2012Article
- A novel virulence strategy for Pseudomonas aeruginosa mediated by an autotransporter with arginine-specific aminopeptidase activity.PLoS pathogens · 2012Article
- Cleavage of IgG1 and IgG3 by gingipain K from Porphyromonas gingivalis may compromise host defense in progressive periodontitis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2011Article
- Smoking and periodontal disease: discrimination of antibody responses to pathogenic and commensal oral bacteria.Clinical and experimental immunology · 2011Article
- Porphyromonas gingivalis-dendritic cell interactions: consequences for coronary artery disease.Journal of oral microbiology · 2010Article
- Dichotomy of gingipains action as virulence factors: from cleaving substrates with the precision of a surgeon's knife to a meat chopper-like brutal degradation of proteins.Periodontology 2000 · 2010Review
- The native 67-kilodalton minor fimbria of Porphyromonas gingivalis is a novel glycoprotein with DC-SIGN-targeting motifs.Journal of bacteriology · 2010Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Gingipains are cysteine proteinases produced by Porphyromonas gingivalis, a major causative bacterium of adult periodontitis. They consist of arginine-specific (HRgpA and RgpB) and lysine-specific (Kgp) proteinases. Gingipains strongly affect the host defense system by degrading some cytokines, components of the complement system, and several immune cell receptors. In an in vitro model, gingipains were shown to degrade soluble tumor necrosis factor alpha (TNF-alpha). However, since membrane TNF-alpha shows strong biological activity, especially in local inflammatory lesions, it was worth investigating whether gingipains might also destroy membrane TNF-alpha and limit its biological activities. To avoid a possible influence of gingipains on ADAM17, the secretase of TNF-alpha, the majority of experiments were performed using ADAM17-/- fibroblasts stably transfected with cDNA of human pro-TNF-alpha (ADAM17-/- TNF+). Arginine-specific gingipains (Rgp's) strongly diminished the level of TNF-alpha on the cell surface as measured by flow cytometry, and this process was not accompanied by an increased concentration of soluble TNF-alpha in the culture medium. Degradation of membrane TNF-alpha by Rgp's correlated with a strong decrease in TNF-alpha-mediated biological activities of ADAM17-/- TNF+ cells. First, the activation state of transcription factor NF-kappaB was suppressed; second, the cells were no longer able to induce apoptosis in HL-60 cells. Kgp was also able to cleave membrane TNF-alpha, but its effect was much weaker than that of Rgp's. Gingipains also limited the binding of native TNF-alpha to the target cells. Thus, gingipains are able not only to cleave soluble TNF-alpha but also to destroy the membrane form of the cytokine, which may additionally dysregulate the cytokine network.
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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.