ArticleCell host & microbe2014
Porphyromonas gingivalis manipulates complement and TLR signaling to uncouple bacterial clearance from inflammation and promote dysbiosis.
Article in Cell host & microbe, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 271 papers, 1 of them a synthesis that pooled it.
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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
271 citing papers in PubMed, 1 synthesis or guideline pooled it, 410 citations in OpenAlex.
- Systematic review on the role of the gut microbiota in tumors and their treatment.Frontiers in endocrinology · 2024Pooled it
- Oral microbiome modulation mitigates hyperglycemia exacerbation in gestational diabetes mellitus.Nature communications · 2026Trial
- The impact of Lacticaseibacillus paracasei GMNL-143 toothpaste on gingivitis and oral microbiota in adults: a randomized, double-blind, crossover, placebo-controlled trial.BMC oral health · 2024Trial
- Trial
- The protease code of the bacterial gut microbiota: ecological regulation, barrier disruption, and rewiring host defense and signaling.Gut microbes · 2026Review
- Magnesium Enhances Immune Clearance of P. gingivalis in Macrophages by Suppressing MCU-Mediated Mitochondrial Calcium Overload.Cell proliferation · 2026Article
- Polymicrobial-driven NLRP6 inflammasome regulates IL-1β production and alveolar bone loss in a murine model of periodontitis.PLoS pathogens · 2026Article
- Impact of periodontitis on the efficacy of neoadjuvant immunochemotherapy in non-small cell lung cancer: a multi-center real-world study.International journal of clinical oncology · 2026Article
- Article
- Spatiotemporal immunomodulation with programmable biomaterials to promote musculoskeletal tissue regeneration.Bioactive materials · 2026Review
- Article
- Platelet-derived concentrates in the immunological management of periodontitis: from dysbiosis to personalized approaches.Odontology · 2026Review
- Supramolecular strategy for compartment pathogen clearance and immuno-metabolic homeostasis to treat periodontitis.Nature communications · 2026Article
- The Role of Oral Pathobionts' Outer Membrane Vesicles in Cancer Pathology and Therapeutic Development.Cells · 2026Review
- Resveratrol supplementation as a non-surgical treatment in periodontitis and related systemic conditions.Journal of traditional and complementary medicine · 2026Review
- A CRISPR array orchestrates virulence and host response inMicrobiology spectrum · 2026Article
- An Oxygen-Releasing Mouthwash Reduces Porphyromonas gingivalis Biofilm and Suppresses fimA and hagA Expression.International dental journal · 2026Article
- Neutrophil Activation Decreases Ability to Kill Oral Streptococcus gordonii.Molecular oral microbiology · 2026Article
- Porphyromonas gingivalis Suppresses Interferon-Gamma Signaling in Macrophages Through a Contact-Dependent, Gingipain-Mediated Mechanism.MicrobiologyOpen · 2026Article
- Matrix Stiffness Governs Fibroblasts' Regulation of Gingival Immune Homeostasis.Advanced materials (Deerfield Beach, Fla.) · 2026Article
211 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
Abstract
Certain low-abundance bacterial species, such as the periodontitis-associated oral bacterium Porphyromonas gingivalis, can subvert host immunity to remodel a normally symbiotic microbiota into a dysbiotic, disease-provoking state. However, such pathogens also exploit inflammation to thrive in dysbiotic conditions. How these bacteria evade immunity while maintaining inflammation is unclear. As previously reported, P. gingivalis remodels the oral microbiota into a dysbiotic state by exploiting complement. Now we show that in neutrophils P. gingivalis disarms a host-protective TLR2-MyD88 pathway via proteasomal degradation of MyD88, whereas it activates an alternate TLR2-Mal-PI3K pathway. This alternate TLR2-Mal-PI3K pathway blocks phagocytosis, provides "bystander" protection to otherwise susceptible bacteria, and promotes dysbiotic inflammation in vivo. This mechanism to disengage bacterial clearance from inflammation required an intimate crosstalk between TLR2 and the complement receptor C5aR and can contribute to the persistence of microbial communities that drive dysbiotic diseases.
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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.