ArticleToxins2010
Porphyromonas gingivalis gingipains trigger a proinflammatory response in human monocyte-derived macrophages through the p38α mitogen-activated protein kinase signal transduction pathway.
Article in Toxins, 2010. 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.
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Who cites it
26 citing papers in PubMed, 36 citations in OpenAlex.
- The Microbial Mechanisms of Cardiovascular Disease: Oral Dysbiosis as a Systemic Instigator.Journal of cardiovascular translational research · 2026Review
- Novel small molecule targeting PgQC reducesFrontiers in oral health · 2026Article
- Review
- Emerging therapeutic strategies targeting bone signaling pathways in periodontitis.Journal of periodontal research · 2025Review
- Article
- The immunomodulatory and antitumor properties of the bacterial metalloprotease Oligopeptidase A are mediated by TLR4/MyD88/TRIF and MAPK signaling pathways.Frontiers in immunology · 2025Article
- Multifunctional role of oral bacteria in the progression of non-alcoholic fatty liver disease.World journal of hepatology · 2024Review
- Non-coding RNA LINC01010 regulates macrophage polarization and innate immune functions by modulating NFκB signaling pathway.Journal of cellular physiology · 2024Article
- Oral and Gut Microbial Dysbiosis and Non-alcoholic Fatty Liver Disease: The Central Role ofFrontiers in medicine · 2022Review
- Gestational diabetes and the human salivary microbiota: a longitudinal study during pregnancy and postpartum.BMC pregnancy and childbirth · 2020Observational
- Gingipain of Porphyromonas gingivalis manipulates M1 macrophage polarization through C5a pathway.In vitro cellular & developmental biology. Animal · 2017Article
- Porphyromonas gingivalis gingipains cause defective macrophage migration towards apoptotic cells and inhibit phagocytosis of primary apoptotic neutrophils.Cell death & disease · 2017Article
- Porphyromonas gingivalis activates NFκB and MAPK pathways in human oral epithelial cells.BMC immunology · 2017Article
- Article
- Enzyme-labeled Antigen Method: Development and Application of the Novel Approach for Identifying Plasma Cells Locally Producing Disease-specific Antibodies in Inflammatory Lesions.Acta histochemica et cytochemica · 2016Review
- Gingipains from Porphyromonas gingivalis promote the transformation and proliferation of vascular smooth muscle cell phenotypes.International journal of clinical and experimental medicine · 2015Article
- In situ visualization of plasma cells producing antibodies reactive to Porphyromonas gingivalis in periodontitis: the application of the enzyme-labeled antigen method.Molecular oral microbiology · 2014Article
- Gingipains from Porphyromonas gingivalis play a significant role in induction and regulation of CXCL8 in THP-1 cells.BMC microbiology · 2014Article
- Hemoglobin receptor protein from Porphyromonas gingivalis induces interleukin-8 production in human gingival epithelial cells through stimulation of the mitogen-activated protein kinase and NF-κB signal transduction pathways.Infection and immunity · 2014Article
- Activation of NLRP3 and AIM2 inflammasomes by Porphyromonas gingivalis infection.Infection and immunity · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Porphyromonas gingivalis, the major etiologic agent of chronic periodontitis, produces a broad spectrum of virulence factors, including Arg- and Lys-gingipain cysteine proteinases. In this study, we investigated the capacity of P. gingivalis gingipains to trigger a proinflammatory response in human monocyte-derived macrophages. Both Arg- and Lys-gingipain preparations induced the secretion of TNF-α and IL-8 by macrophages. Stimulation of macrophages with Arg-gingipain A/B preparation at the highest concentration was associated with lower amounts of cytokines detected, a phenomenon likely related to proteolytic degradation. The inflammatory response induced by gingipains was not dependent of their catalytic activity since heat-inactivated preparations were still effective. Stimulating macrophages with gingipain preparations was associated with increased levels of phosphorylated p38α MAPK suggesting its involvement in cell activation. In conclusion, our study brought clear evidence that P. gingivalis Arg- and Lys-gingipains may contribute to the host inflammatory response, a critical factor in periodontitis-associated tissue destruction.
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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.