ArticleACS nano2014
Interference in autophagosome fusion by rare earth nanoparticles disrupts autophagic flux and regulation of an interleukin-1β producing inflammasome.
Article in ACS nano, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 154 citations in OpenAlex.
- Pulmonary toxicity of brake wear particles: effects of composition and surface reactivity.Particle and fibre toxicology · 2026Article
- pH sensing and inflammation: linking acidic microenvironments to immune reprogramming.Frontiers in immunology · 2026Review
- Deferential nephrotoxicity effect of lanthanum oxide nanoparticle responses to concentration and time in vivo.Scientific reports · 2025Article
- Genetic modulation of rare earth nanoparticle biotransformation shapes biological outcomes.Nature communications · 2025Article
- The role of NLRP3 inflammasome activation in proinflammatory and cytotoxic effects of metal nanoparticles.Archives of toxicology · 2025Review
- Deciphering key nano-bio interface descriptors to predict nanoparticle-induced lung fibrosis.Particle and fibre toxicology · 2025Article
- Article
- Virus-Shaped Mesoporous Silica Nanostars to Improve the Transport of Drugs across the Blood-Brain Barrier.ACS applied materials & interfaces · 2024Article
- A phosphatase-like nanomaterial promotes autophagy and reprograms macrophages for cancer immunotherapy.Chemical science · 2024Article
- Zinc oxide nanoparticles exacerbate skin epithelial cell damage by upregulating pro-inflammatory cytokines and exosome secretion in M1 macrophages following UVB irradiation-induced skin injury.Particle and fibre toxicology · 2024Article
- The deposition of lanthanum carbonate may activate macrophages to induce gastrointestinal mucosal injury in patients with chronic kidney disease: an in vitro caco-2/THP-1 macrophage coculture model study.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2024Article
- Macrophage-based therapeutic approaches for cardiovascular diseases.Basic research in cardiology · 2024Review
- Approaches to Nanoparticle Labeling: A Review of Fluorescent, Radiological, and Metallic Techniques.Environment & health (Washington, D.C.) · 2023Review
- Modulating Nanozyme-Based Nanomachines via Microenvironmental Feedback for Differential Photothermal Therapy of Orthotopic Gliomas.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Mechanisms of cell injury induced by inhaled molybdenum trioxide nanoparticles in Golden Syrian Hamsters.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- Diverse Pathways of Engineered Nanoparticle-Induced NLRP3 Inflammasome Activation.Nanomaterials (Basel, Switzerland) · 2022Review
- NOX2-mediated reactive oxygen species are double-edged swords in focal cerebral ischemia in mice.Journal of neuroinflammation · 2022Article
- TFEB-lysosome pathway activation is associated with different cell death responses to carbon quantum dots in Kupffer cells and hepatocytes.Particle and fibre toxicology · 2022Article
- Understanding Nanomaterial-Liver Interactions to Facilitate the Development of Safer Nanoapplications.Advanced materials (Deerfield Beach, Fla.) · 2022Review
- Rare earth smart nanomaterials for bone tissue engineering and implantology: Advances, challenges, and prospects.Bioengineering & translational medicine · 2022Review
1 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Engineered nanomaterials (ENMs) including multiwall carbon nanotubes (MWCNTs) and rare earth oxide (REO) nanoparticles, which are capable of activating the NLRP3 inflammasome and inducing IL-1β production, have the potential to cause chronic lung toxicity. Although it is known that lysosome damage is an upstream trigger in initiating this pro-inflammatory response, the same organelle is also an important homeostatic regulator of activated NLRP3 inflammasome complexes, which are engulfed by autophagosomes and then destroyed in lysosomes after fusion. Although a number of ENMs have been shown to induce autophagy, no definitive research has been done on the homeostatic regulation of the NLRP3 inflammasome during autophagic flux. We used a myeloid cell line (THP-1) and bone marrow derived macrophages (BMDM) to compare the role of autophagy in regulating inflammasome activation and IL-1β production by MWCNTs and REO nanoparticles. THP-1 cells express a constitutively active autophagy pathway and are also known to mimic NLRP3 activation in pulmonary macrophages. We demonstrate that, while activated NLRP3 complexes could be effectively removed by autophagosome fusion in cells exposed to MWCNTs, REO nanoparticles interfered in autophagosome fusion with lysosomes. This leads to the accumulation of the REO-activated inflammasomes, resulting in robust and sustained IL-1β production. The mechanism of REO nanoparticle interference in autophagic flux was clarified by showing that they disrupt lysosomal phosphoprotein function and interfere in the acidification that is necessary for lysosome fusion with autophagosomes. Binding of LaPO4 to the REO nanoparticle surfaces leads to urchin-shaped nanoparticles collecting in the lysosomes. All considered, these data demonstrate that in contradistinction to autophagy induction by some ENMs, specific materials such as REOs interfere in autophagic flux, thereby disrupting homeostatic regulation of activated NLRP3 complexes.
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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.