ArticlePLoS pathogens2013
The serine phosphatase SerB of Porphyromonas gingivalis suppresses IL-8 production by dephosphorylation of NF-κB RelA/p65.
Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
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Who cites it
75 citing papers in PubMed, 103 citations in OpenAlex.
- A Dusty Affair: SIRT1-S682 Modulation Orchestrates ERK-FN1-p38-NF-κB Signaling and Composite-Dependent IL-8 Responses in Gingival Keratinocytes Exposed to Dental Dust and Eluates.Journal of functional biomaterials · 2026Article
- A CRISPR array orchestrates virulence and host response inMicrobiology spectrum · 2026Article
- The survival status ofJournal of oral microbiology · 2026Review
- Crossroads of well-being: oral health, neurology, neuronutrition and healthy aging.Open medicine (Warsaw, Poland) · 2026Review
- Tyrosine phosphorylation coupling of one-carbon metabolism and virulence in an endogenous pathogen.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Hypoxia drives progression of multiple sclerosis by enhancing the inflammasome activation in macrophages with Porphyromonas gingivalis infection.Cell death discovery · 2025Article
- Article
- Role of the oral-gut microbiota axis in pancreatic cancer: a new perspective on tumor pathophysiology, diagnosis, and treatment.Molecular medicine (Cambridge, Mass.) · 2025Review
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- The Impact of E-Cigarettes on Oral Health-A Narrative Review.Dentistry journal · 2024Review
- MbovP0725, a secreted serine/threonine phosphatase, inhibits the host inflammatory response and affects metabolism inmSystems · 2024Article
- Post-translational modifications of p65: state of the art.Frontiers in cell and developmental biology · 2024Review
- Arginine-specific gingipains (RgpA/RgpB) knockdown modulates neutrophil machinery.Journal of oral microbiology · 2024Article
- Chronological analysis of periodontal bone loss in experimental periodontitis in mice.Clinical and experimental dental research · 2023Article
- Social networking at the microbiome-host interface.Infection and immunity · 2023Review
- Illuminating the oral microbiome: cellular microbiology.FEMS microbiology reviews · 2023Article
- Cigarette smoke extract impairs gingival epithelial barrier function.Scientific reports · 2023Article
- Molecular systems architecture of host-microbiome interactions in periodontitis.JADA foundational science · 2023Review
- Current concepts in the pathogenesis of periodontitis: from symbiosis to dysbiosis.Journal of oral microbiology · 2023Review
- Coilin as a regulator of NF-kB mediated inflammation in preeclampsia.Biology open · 2022Article
15 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Porphyromonas gingivalis is a major pathogen in severe and chronic manifestations of periodontal disease, which is one of the most common infections of humans. A central feature of P. gingivalis pathogenicity is dysregulation of innate immunity at the gingival epithelial interface, including suppression of IL-8 production by epithelial cells. NF-κB is a transcriptional regulator that controls important aspects of innate immune responses, and NF-κB RelA/p65 homodimers regulate transcription of IL8. Phosphorylation of the NF-κB p65 subunit protein on the serine 536 residue affects nuclear translocation and transcription of target genes. Here we show that SerB, a haloacid dehalogenase (HAD) family serine phosphatase secreted by P. gingivalis, is produced intracellularly and can specifically dephosphorylate S536 of p65 in gingival epithelial cells. A P. gingivalis mutant lacking SerB was impaired in dephosphorylation of p65 S536, and ectopically expressed SerB bound to p65 and co-localized with p65 in the cytoplasm. Ectopic expression of SerB also resulted in dephosphorylation of p65 with reduced nuclear translocation in TNF-α-stimulated epithelial cells. In contrast, the p105/50 subunit of NF-κB was unaffected by SerB. Co-expression of a constitutively active p65 mutant (S536D) relieved inhibition of nuclear translocation. Both the activity of the IL8 promoter and production of IL-8 were diminished by SerB. Deletion and truncation mutants of SerB lacking the HAD-family enzyme motifs of SerB were unable to dephosphorylate p65, inhibit nuclear translocation or abrogate IL8 transcription. Specific dephosphorylation of NF-κB p65 S536 by SerB, and consequent inhibition of nuclear translocation, provides the molecular basis for a bacterial strategy to manipulate host inflammatory pathways and repress innate immunity at mucosal surfaces.
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