ArticleScientific reports2016
Microbial Degradation of Cellular Kinases Impairs Innate Immune Signaling and Paracrine TNFα Responses.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Interspecies regulation of virulence through gingipain inhibition by a Tannerella forsythia serpin.EMBO reports · 2026Article
- Lys-specific gingipain (Kgp) ofmBio · 2025Article
- Influences of bacterial extracellular vesicles on macrophage immune functions.Frontiers in cellular and infection microbiology · 2024Review
- Microbiome-mediated incapacitation of interferon lambda production in the oral mucosa.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Article
- Multiple roles of caspase-8 in cell death, inflammation, and innate immunity.Journal of leukocyte biology · 2021Review
- Diet-Induced Non-alcoholic Fatty Liver Disease and Associated Gut Dysbiosis Are Exacerbated by Oral Infection.Frontiers in oral health · 2021Article
- Nano-based approach to combat emerging viral (NIPAH virus) infection.Nanomedicine : nanotechnology, biology, and medicine · 2019Review
- Transcriptome analysis of Porphyromonas gingivalis and Acinetobacter baumannii in polymicrobial communities.Molecular oral microbiology · 2018Article
- Identification of Streptococcus cristatus peptides that repress expression of virulence genes in Porphyromonas gingivalis.Scientific reports · 2017Article
- Genes Contributing toFrontiers in cellular and infection microbiology · 2017Article
- Inactive Gingipains fromFrontiers in cellular and infection microbiology · 2017Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The NFκB and MAPK signaling pathways are critical components of innate immunity that orchestrate appropriate immune responses to control and eradicate pathogens. Their activation results in the induction of proinflammatory mediators, such as TNFα a potent bioactive molecule commonly secreted by recruited inflammatory cells, allowing for paracrine signaling at the site of an infection. In this study we identified a novel mechanism by which the opportunistic pathogen Porphyromonas gingivalis dampens innate immune responses by disruption of kinase signaling and degradation of inflammatory mediators. The intracellular immune kinases RIPK1, TAK1, and AKT were selectively degraded by the P. gingivalis lysine-specific gingipain (Kgp) in human endothelial cells, which correlated with dysregulated innate immune signaling. Kgp was also observed to attenuate endothelial responsiveness to TNFα, resulting in a reduction in signal flux through AKT, ERK and NFκB pathways, as well as a decrease in downstream proinflammatory mRNA induction of cytokines, chemokines and adhesion molecules. A deficiency in Kgp activity negated decreases to host cell kinase protein levels and responsiveness to TNFα. Given the essential role of kinase signaling in immune responses, these findings highlight a unique mechanism of pathogen-induced immune dysregulation through inhibition of cell activation, paracrine signaling, and dampened cellular proinflammatory responses.
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