ArticlePloS one2013
Porphyromonas gingivalis regulates TREM-1 in human polymorphonuclear neutrophils via its gingipains.
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 36 papers.
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Who cites it
36 citing papers in PubMed, 61 citations in OpenAlex.
- Pathogenicity ofFrontiers in cellular and infection microbiology · 2026Article
- TREM-1 Pathway Biomarkers for Classification of Periodontal Diseases and Monitoring of Treatment Response in Grade B and C Periodontitis.Journal of clinical periodontology · 2025Article
- Article
- Arginine-specific gingipains (RgpA/RgpB) knockdown modulates neutrophil machinery.Journal of oral microbiology · 2024Article
- Salivary secretory leukocyte protease inhibitor levels in patients with stage 3 grade C periodontitis: a comparative cross-sectional study.Scientific reports · 2022Article
- The subversion of toll-like receptor signaling by bacterial and viral proteases during the development of infectious diseases.Molecular aspects of medicine · 2022Review
- Anti-Inflammatory Effect of Charantadiol A, Isolated from Wild Bitter Melon Leaf, on Heat-InactivatedMolecules (Basel, Switzerland) · 2021Article
- Elevated serum TREM-1 is associated with periodontitis and disease activity in rheumatoid arthritis.Scientific reports · 2021Observational
- Porphyromonas gingivalis gingipains potentially affect MUC5AC gene expression and protein levels in respiratory epithelial cells.FEBS open bio · 2021Article
- Severe Periodontitis and Biomarkers of Bacterial Burden. Results From a Case-Control and Intervention Clinical Trial.Frontiers in oral health · 2021Article
- Periodontitis Exacerbates and Promotes the Progression of Chronic Kidney Disease Through Oral Flora, Cytokines, and Oxidative Stress.Frontiers in microbiology · 2021Review
- Porphyromonas gingivalis adopts intricate and unique molecular mechanisms to survive and persist within the host: a critical update.Journal of oral microbiology · 2020Review
- The modulation of the TREM-1/PGLYRP1/MMP-8 axis in peri-implant diseases.Clinical oral investigations · 2020Article
- Proteolysis of Gingival Keratinocyte Cell Surface Proteins by Gingipains Secreted FromFrontiers in microbiology · 2020Article
- TREM-1 Is Upregulated in Experimental Periodontitis, and Its Blockade Inhibits IL-17A and RANKL Expression and Suppresses Bone loss.Journal of clinical medicine · 2019Article
- Novel Assay To Characterize Neutrophil Responses to Oral Biofilms.Infection and immunity · 2019Article
- Article
- Apoptosis Transcriptional Profile Induced byMediators of inflammation · 2019Article
- Gingival Exudatome Dynamics Implicate Inhibition of the Alternative Complement Pathway in the Protective Action of the C3 Inhibitor Cp40 in Nonhuman Primate Periodontitis.Journal of proteome research · 2018Article
- [Research progress on the relationship between triggering receptor expressed on myeloid cells 1 and 2 and malignant tumors].Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Triggering Receptor Expressed on Myeloid cells 1 (TREM-1) is a cell surface receptor of the immunoglobulin superfamily, with the capacity to amplify pro-inflammatory cytokine production and regulate apoptosis. Polymorphonuclear neutrophils (PMNs) are the first line of defence against infection, and a major source of TREM-1. Porphyromonas gingivalis is a Gram-negative anaerobe highly implicated in the inflammatory processes governing periodontal disease, which is characterized by the destruction of the tooth-supporting tissues. It expresses a number of virulence factors, including the cysteine proteinases (or gingipains). The aim of this in vitro study was to investigate the effect of P. gingivalis on TREM-1 expression and production by primary human PMNs, and to evaluate the role of its gingipains in this process. After 4 h of challenge, P. gingivalis enhanced TREM-1 expression as identified by quantitative real-time PCR. This was followed by an increase in soluble (s)TREM-1 secretion over a period of 18 h, as determined by ELISA. At this time-point, the P. gingivalis-challenged PMNs exhibited diminished TREM-1 cell-membrane staining, as identified by flow cytometry and confocal laser scanning microscopy. Furthermore engagement of TREM-1, by means of anti-TREM-1 antibodies, enhanced the capacity of P. gingivalis to stimulate interleukin (IL)-8 production. Conversely, antagonism of TREM-1 using a synthetic peptide resulted in reduction of IL-8 secretion. Using isogenic P. gingivalis mutant strains, we identified the Arg-gingipain to be responsible for shedding of sTREM-1 from the PMN surface, whereas the Lys-gingipain had the capacity to degrade TREM-1. In conclusion, the differential regulation of TREM-1 by the P. gingivalis gingipains may present a novel mechanism by which P. gingivalis manipulates the host innate immune response helping to establish chronic periodontal inflammation.
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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.