ArticleInternational journal of oral science2018
Streptococcus mutans activates the AIM2, NLRP3 and NLRC4 inflammasomes in human THP-1 macrophages.
Article in International journal of oral science, 2018. 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, 26 citations in OpenAlex.
- Redefining the Evolution of Pulpal Pathology: Inflammasomes as Central Integrative Hubs and Biological Switches Governing the Transition From Reversible to Irreversible Pulpal Inflammation Beyond Symptom-Based Classification.International endodontic journal · 2026Review
- Streptococcus anginosus activates the NLRP3 inflammasome to promote inflammatory responses from macrophages.Journal of leukocyte biology · 2026Article
- Harnessing Microbiome-Mediated and Macrophage-Driven Mechanisms for Oral Wound Healing.Microorganisms · 2026Review
- Serotype and distribution of adhesion genes in Streptococcus mutans isolated from people with Parkinson's disease.Odontology · 2025Article
- Roles of Pyroptosis in the Progression of Pulpitis and Apical Periodontitis.Journal of inflammation research · 2025Review
- Development of a Coculture Model for Assessing Competing Host Mammalian Cell and Bacterial Attachment on Zirconia versus Titanium.ACS biomaterials science & engineering · 2024Article
- NLRP3 inflammasome activity and periodontal disease pathogenesis-A bidirectional relationship.Oral diseases · 2024Review
- Emerging targets signaling for inflammation in Parkinson's disease drug discovery.Metabolic brain disease · 2022Review
- Infective Endocarditis in High-Income Countries.Metabolites · 2022Review
- AIM2 Inflammasome's First Decade of Discovery: Focus on Oral Diseases.Frontiers in immunology · 2020Review
- Key Mechanisms and Potential Targets of the NLRP3 Inflammasome in Neurodegenerative Diseases.Frontiers in integrative neuroscience · 2020Review
- Bacterial Type I CRISPR-Cas systems influence inflammasome activation in mammalian host by promoting autophagy.Immunology · 2019Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Streptococcus mutans (S. mutans), a major aetiologic agent of dental caries, is involved in systemic diseases, such as bacterial endocarditis, if it enters the bloodstream through temporary bacteraemia. Interleukin (IL)-1β, a proinflammatory cytokine, is related to the host defences against pathogens, and its synthesis, maturation, and secretion are tightly regulated by the activation of the inflammasome, an inflammatory signalling complex. This study examined the signalling mechanism of IL-1β secretion and the inflammasome pathway induced by S. mutans to explain the molecular mechanism through which systemic infection by oral streptococci can occur. After infection of THP-1 cells with S. mutans, the expression of inflammasome components was detected using various methods. S. mutans induced IL-1β secretion via caspase-1 activation, and S. mutans-induced IL-1β secretion required absent in melanoma (AIM2), NLR family pyrin domain-containing 3 (NLRP3) and NLR family CARD domain-containing 4 (NLRC4) inflammasome activation. In particular, the S. mutans-induced NLRP3 inflammasome was mediated by adenosine triphosphate (ATP) release, potassium depletion and lysosomal damage. Our study provides novel insight into the innate immune response against S. mutans infection.
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