ArticleInnate immunity2014
Inflammatory response to Porphyromonas gingivalis partially requires interferon regulatory factor (IRF) 3.
Article in Innate immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
The trial behind it
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
17 citing papers in PubMed, 17 citations in OpenAlex.
- ROR2 preserves alveolar bone homeostasis by orchestrating IRAK4-dependent suppression of CXCL8-driven osteolysis.Cell communication and signaling : CCS · 2026Article
- Genome-wide profiling of salivary promoter-region DNA methylation in periodontitis: the Tromsø Study.BMC medical genomics · 2026Article
- Altered microRNA expression correlates with reduced TLR2/4-dependent periodontal inflammation and bone resorption induced by polymicrobial infection.Microbiology spectrum · 2025Article
- CRISPRJournal of oral microbiology · 2025Article
- IRF3 Promotes Production of IL-6 and Nitric Oxide but Represses CCL22 in RAW264.7 Macrophage Cells Exposed to Lipopolysaccharides in Culture.Journal of inflammation research · 2025Article
- How Do Microorganisms Influence the Development of Endometriosis? Participation of Genital, Intestinal and Oral Microbiota in Metabolic Regulation and Immunopathogenesis of Endometriosis.International journal of molecular sciences · 2023Review
- Oral microbiome mediated inflammation, a potential inductor of vascular diseases: a comprehensive review.Frontiers in cardiovascular medicine · 2023Review
- Is There an Interplay between Oral Microbiome, Head and Neck Carcinoma and Radiation-Induced Oral Mucositis?Cancers · 2021Review
- Implication of Toll/IL-1 receptor domain containing adapters inInnate immunity · 2021Article
- A therapeutic oxygen carrier isolated from Arenicola marina decreased P. gingivalis induced inflammation and tissue destruction.Scientific reports · 2020Article
- The Anti-Inflammatory Effects of Shinbaro3 Is Mediated by Downregulation of the TLR4 Signalling Pathway in LPS-Stimulated RAW 264.7 Macrophages.Mediators of inflammation · 2018Article
- Article
- Porphyromonas gingivalis-mediated signaling through TLR4 mediates persistent HIV infection of primary macrophages.Virology · 2016Article
- Liver X receptors contribute to periodontal pathogen-elicited inflammation and oral bone loss.Molecular oral microbiology · 2015Article
- The interferon regulatory factors as novel potential targets in the treatment of cardiovascular diseases.British journal of pharmacology · 2015Review
- Aging and contribution of MyD88 and TRIF to expression of TLR pathway-associated genes following stimulation with Porphyromonas gingivalis.Journal of periodontal research · 2015Article
- Immuno-pathogenesis of Periodontal Disease: Current and Emerging Paradigms.Current oral health reports · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Innate immune activation with expression of pro-inflammatory molecules such as TNF-α is a hallmark of the chronic inflammation associated with periodontal disease (PD). Porphyromonas gingivalis, a bacterium associated with PD, engages TLRs and activates MyD88-dependent and TIR-domain-containing adapter-inducing IFN-β (TRIF)-dependent signaling pathways. IFN regulatory factor (IRF) 3 is activated in a TRIF-dependent manner and participates in production of cytokines such as TNF-α; however, little is known regarding IRF3 and the host response to PD pathogens. We speculated that IRF3 participates in the host inflammatory response to P. gingivalis. Our results show that bone marrow macrophages (MØ) from WT mice respond to P. gingivalis with activation and nuclear translocation of IRF3. Compared with WT, MØ from IRF3(-/-), TRIF(-/-), and TLR4(-/-) mice responded with reduced levels of TNF-α on P. gingivalis challenge. In addition, full expression of IL-6 and RANTES by MØ to P. gingivalis was dependent on IRF3. Lastly, employing MØ from IRF3(-/-) and IRF7(-/-) mice we observed a significant role for IRF3 and a modest role for IRF7 in the P. gingivalis-elicited TNF-α response. These studies identify a role for IRF3 in the inflammatory response by MØ to the periodontal pathogen P. gingivalis.
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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.