ArticleCell death & disease2015
The NLRP3 inflammasome is activated by nanoparticles through ATP, ADP and adenosine.
Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers, 1 of them a synthesis that pooled it.
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Who cites it
103 citing papers in PubMed, 1 synthesis or guideline pooled it, 211 citations in OpenAlex.
- Analyzing Molecular Determinants of Nanodrugs' Cytotoxic Effects.International journal of molecular sciences · 2025Pooled it
- NLRP3 inflammasome activation by particles and fibers: implications for human hazard assessment.Archives of toxicology · 2026Review
- Damage-Associated Molecular Patterns in Mesothelioma: Drivers of Inflammation and Therapeutic Targets.International journal of molecular sciences · 2026Review
- Prognostic significance of calcium signaling-related genes in bladder cancer and the role of ATP2B4 in regulating mitochondrial calcium ion levels via the VDAC1/MCU pathway.Frontiers in immunology · 2026Article
- Nanotoxicity of Porous Silica Nanoparticles: Physicochemical Properties and Mechanistic Cellular Endpoints.Nanomaterials (Basel, Switzerland) · 2025Review
- Review
- Ghrelin Inhibits Inflammasomes Activation in Astrocytes, Alleviates Pyroptosis, and Prevents Lipopolysaccharide-induced Depression-like Behavior in Mice.Inflammation · 2025Article
- IL-33-primed NLRP3 inflammasome in basophils drives IL-1β production and initiates atopic dermatitis inflammation.Cell death discovery · 2025Article
- Effects of Caffeine on THP-1 Myelogenous Cell Inflammatory Gene Expression.Current issues in molecular biology · 2025Article
- The role of NLRP3 inflammasome activation in proinflammatory and cytotoxic effects of metal nanoparticles.Archives of toxicology · 2025Review
- Impact of ionizable groups in star polymer nanoparticles on NLRP3 inflammasome activation.Biomaterials science · 2025Article
- Mechanisms of mitochondrial damage-associated molecular patterns associated with inflammatory response in cardiovascular diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Human Primary Monocytes as a Model for in vitro Immunotoxicity Testing: Evaluation of the Regulatory Properties of TiOInternational journal of nanomedicine · 2025Article
- Beyond cytotoxicity: pollutant mixtures elicit unconventional epithelial-fibroblast signaling in a human lung air-liquid interface co-culture model.Frontiers in toxicology · 2025Article
- Silver nanoparticle induced immunogenic cell death can improve immunotherapy.Journal of nanobiotechnology · 2024Article
- Activation of osmo-sensitive LRRC8 anion channels in macrophages is important for micro-crystallin joint inflammation.Nature communications · 2024Article
- Varying the hydrophobic core composition of polymeric nanoparticles affects NLRP3 inflammasome activation.Biomaterials science · 2024Article
- Polyethylene Terephthalate Microplastics Generated from Disposable Water Bottles Induce Interferon Signaling Pathways in Mouse Lung Epithelial Cells.Nanomaterials (Basel, Switzerland) · 2024Article
- Article
- Crosstalk between P2Y receptors and cyclooxygenase activity in inflammation and tissue repair.Purinergic signalling · 2024Review
43 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The NLR pyrin domain containing 3 (NLRP3) inflammasome is a major component of the innate immune system, but its mechanism of activation by a wide range of molecules remains largely unknown. Widely used nano-sized inorganic metal oxides such as silica dioxide (nano-SiO2) and titanium dioxide (nano-TiO2) activate the NLRP3 inflammasome in macrophages similarly to silica or asbestos micro-sized particles. By investigating towards the molecular mechanisms of inflammasome activation in response to nanoparticles, we show here that active adenosine triphosphate (ATP) release and subsequent ATP, adenosine diphosphate (ADP) and adenosine receptor signalling are required for inflammasome activation. Nano-SiO2 or nano-TiO2 caused a significant increase in P2Y1, P2Y2, A2A and/or A2B receptor expression, whereas the P2X7 receptor was downregulated. Interestingly, IL-1β secretion in response to nanoparticles is increased by enhanced ATP and ADP hydrolysis, whereas it is decreased by adenosine degradation or selective A2A or A2B receptor inhibition. Downstream of these receptors, our results show that nanoparticles activate the NLRP3 inflammasome via activation of PLC-InsP3 and/or inhibition of adenylate cyclase (ADCY)-cAMP pathways. Finally, a high dose of adenosine triggers inflammasome activation and IL-1β secretion through adenosine cellular uptake by nucleotide transporters and by its subsequent transformation in ATP by adenosine kinase. In summary, we show for the first time that extracellular adenosine activates the NLRP3 inflammasome by two ways: by interacting with adenosine receptors at nanomolar/micromolar concentrations and through cellular uptake by equilibrative nucleoside transporters at millimolar concentrations. These findings provide new molecular insights on the mechanisms of NLRP3 inflammasome activation and new therapeutic strategies to control inflammation.
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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.