ArticleInflammation2025
Quorum Sensing Molecule Autoinducer-2 Promotes Macrophage Classical Polarization and Exacerbates Periodontal Inflammation Via Nf-Κb Signalling.
Article in Inflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Quorum Sensing and Quorum Quenching in Periodontal Disease: Mechanisms and Therapeutic Potential.Current issues in molecular biology · 2026Review
- Quorum sensing in oral multispecies biofilms: from interkingdom communication to therapeutic targeting.Frontiers in microbiology · 2026Review
- Curcumin-alendronate carbon dots: A dual-logic strategy for precision treatment of periodontitis.Materials today. Bio · 2025Article
- Autoinducer-2 signaling promotes intestinal colonization ofApplied and environmental microbiology · 2025Article
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Authors and funding
6 authors.
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Abstract
backgroundThe role of quorum sensing signaling in the immunoinflammatory response during the development of periodontitis is not yet known. This study aimed to explore the effect of Autoinducer-2, a quorum sensing signaling molecule, on macrophage phenotypic remodeling in the immune microenvironment of periodontitis, to further elucidate its mechanism and to discover inhibitors against periodontitis.
methodsBioluminescence experiments and periodontitis model were used to demonstrate the association between periodontitis progression with AI-2. Next, AI-2 challenged macrophage was introduced to transcriptomic sequence and the immune profile was characterized in combination with flow cytometry, qPCR, and immunofluorescence. Activation of NF-κB signalling by AI-2 was confirmed by fluorescence co-localization and immunoblotting. Finally, morphological methods such as Micro-CT and HE, TRAP staining and immunological methods such as immunohistochemistry/fluorescence staining were used to assess the mechanisms by which AI-2 regulates periodontitis progression.
resultsAI-2 level was positively correlated with the progression of periodontitis stages and was significantly higher in periodontitis stage III and IV patients. AI-2 promotes macrophage classical polarization and facilitates the secretion of inflammatory factors in vitro, which is dependent on the activation of the NF-κB signaling pathway. AI-2 promotes alveolar bone resorption, but D-ribose acts as a quorum sensing inhibitor to alleviate macrophage classical polarization and attenuates alveolar bone resorption and inflammatory responses in periodontitis mice.
conclusionsOur study demonstrates that AI-2 promoted classical polarization of macrophage and exacerbated periodontal inflammation which could be reversed by D-ribose.
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