ArticleMicrobes and infection
NLRX1 modulates differentially NLRP3 inflammasome activation and NF-κB signaling during Fusobacterium nucleatum infection.
Article in Microbes and infection. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 64 citations in OpenAlex.
- Fusobacterium nucleatum in cancer: Interactions with microbiota, tumour colonisation and cancer progression.Clinical and translational medicine · 2026Review
- CircRNA Profiling Identifies hsa_circRNA_003201 Associated with a Predicted NLRX1-Related Regulatory Network in an Acne-Associated Inflammatory Sebocyte Model.Journal of inflammation research · 2026Article
- Harnessing NLRX1: a new frontier in mitigating inflammation in pulmonary hypertension.Respiratory research · 2025Article
- Periodontal pathogens and cancer development.Periodontology 2000 · 2024Review
- Dying for a cause: The pathogenic manipulation of cell death and efferocytic pathways.Molecular oral microbiology · 2024Review
- About a Possible Impact of Endodontic Infections byInternational journal of molecular sciences · 2024Review
- Dynamic dysregulation of transcriptomic networks in brainstem autonomic nuclei during hypertension development in the female spontaneously hypertensive rat.Physiological genomics · 2024Article
- Mitochondrial Dysfunction in Periodontitis and Associated Systemic Diseases: Implications for Pathomechanisms and Therapeutic Strategies.International journal of molecular sciences · 2024Review
- Oral microbiota-host interaction: the chief culprit of alveolar bone resorption.Frontiers in immunology · 2024Review
- Review
- The role of NOD-like receptors in innate immunity.Frontiers in immunology · 2023Review
- [NLRC4 plays a regulatory role in F. nucleatum-induced pyroptosis in macrophages].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
- Nrf2 in the Field of Dentistry with Special Attention to NLRP3.Antioxidants (Basel, Switzerland) · 2022Review
- The Regulatory Effect of Coaggregation BetweenFrontiers in cellular and infection microbiology · 2022Article
- More Than Just a Periodontal Pathogen -the Research Progress onFrontiers in cellular and infection microbiology · 2022Review
- Pathogenic Mechanisms ofFrontiers in oral health · 2022Review
- NLRX1 Deficiency Alters the Gut Microbiome and Is Further Exacerbated by Adherence to a Gluten-Free Diet.Frontiers in immunology · 2022Article
- Sex-Biased Control of Inflammation and Metabolism by a Mitochondrial Nod-Like Receptor.Frontiers in immunology · 2022Article
- Noncoding RNA-mediated regulation of pyroptotic cell death in cancer.Frontiers in oncology · 2022Review
- Physical attributes of salivary calcium particles and their interaction with gingival epithelium.Biomedical journal · 2021Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
Abstract
NOD-like receptors (NLRs) play a large role in regulation of host innate immunity, yet their role in periodontitis remains to be defined. NLRX1, a member of the NLR family that localizes to mitochondria, enhances mitochondrial ROS (mROS) generation. mROS can activate the NLRP3 inflammasome, yet the role of NLRX1 in NLRP3 inflammasome activation has not been examined. In this study, we revealed the mechanism by which NLRX1 positively regulates ATP-induced NLRP3 inflammasome activation through mROS in gingival epithelial cells (GECs). We found that depletion of NLRX1 by shRNA attenuated ATP-induced mROS generation and redistribution of the NLRP3 inflammasome adaptor protein, ASC. Furthermore, depletion of NLRX1 inhibited Fusobacterium nucleatum infection-activated caspase-1, suggesting that it also inhibits the NLRP3 inflammasome. Conversely, NLRX1 also acted as a negative regulator of NF-κB signaling and IL-8 expression. Thus, NLRX1 stimulates detection of the pathogen F. nucleatum via the inflammasome, while dampening cytokine production. We expect that commensals should not activate the inflammasome, and NLRX1 should decrease their ability to stimulate expression of pro-inflammatory cytokines such as IL-8. Therefore, NLRX1 may act as a potential switch with regards to anti-microbial responses in healthy or diseased states in the oral cavity.
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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.