ArticleNanotoxicology2013
IL-33 mediates multi-walled carbon nanotube (MWCNT)-induced airway hyper-reactivity via the mobilization of innate helper cells in the lung.
Article in Nanotoxicology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 2 of them syntheses that pooled it.
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Who cites it
42 citing papers in PubMed, 2 syntheses or guidelines pooled it, 76 citations in OpenAlex.
- Effects of Air Pollution on Lung Innate Lymphoid Cells: Review of In Vitro and In Vivo Experimental Studies.International journal of environmental research and public health · 2019Pooled it
- Meta-analysis of transcriptomic responses as a means to identify pulmonary disease outcomes for engineered nanomaterials.Particle and fibre toxicology · 2016Pooled it
- Impacts of Environmental Pollutants on Innate Immunity: The Role of Group 2 Innate Lymphoid Cells.Clinical reviews in allergy & immunology · 2026Review
- Toward a ToxAtlas of Carbon-Based Nanomaterials: Single-Cell RNA Sequencing Reveals Initiating Cell Circuits in Pulmonary Inflammation.ACS nano · 2025Article
- Article
- Nanoparticle-Induced Airway Eosinophilia Is Independent of ILC2 Signaling but Associated With Sex Differences in Macrophage Phenotype Development.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- COVID-19, an opportunity to reevaluate the correlation between long-term effects of anthropogenic pollutants on viral epidemic/pandemic events and prevalence.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2020Review
- Signaling Pathways Implicated in Carbon Nanotube-Induced Lung Inflammation.Frontiers in immunology · 2020Review
- Polarization of Immune Cells in the Pathologic Response to Inhaled Particulates.Frontiers in immunology · 2020Review
- Microenvironmental Alterations in Carbon Nanotube-Induced Lung Inflammation and Fibrosis.Frontiers in cell and developmental biology · 2020Review
- Sex differences in the inflammatory immune response to multi-walled carbon nanotubes and crystalline silica.Inhalation toxicology · 2019Article
- Multi-walled carbon nanotube oxidation dependent keratinocyte cytotoxicity and skin inflammation.Particle and fibre toxicology · 2019Article
- Pulmonary Exposure to Magnéli Phase Titanium Suboxides Results in Significant Macrophage Abnormalities and Decreased Lung Function.Frontiers in immunology · 2019Article
- Group II innate lymphoid cells and microvascular dysfunction from pulmonary titanium dioxide nanoparticle exposure.Particle and fibre toxicology · 2018Article
- Air pollutants and early origins of respiratory diseases.Chronic diseases and translational medicine · 2018Article
- The Toxicology of Engineered Nanomaterials in Asthma.Current environmental health reports · 2018Review
- Macrophage polarization and activation at the interface of multi-walled carbon nanotube-induced pulmonary inflammation and fibrosis.Nanotoxicology · 2018Article
- Type 2 Immune Mechanisms in Carbon Nanotube-Induced Lung Fibrosis.Frontiers in immunology · 2018Review
- Mechanistic insight into the impact of nanomaterials on asthma and allergic airway disease.Particle and fibre toxicology · 2017Review
- Human peripheral blood mononuclear cells (PBMCs) from smokers release higher levels of IL-1-like cytokines after exposure to combustion-generated ultrafine particles.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Allergic asthma is a chronic inflammatory disorder of the airway associated with bronchial obstruction, airway hyper-reactivity (AHR), and mucus production. The epithelium may direct and propagate asthmatic-like responses. Central to this theory is the observation that viruses, air pollution, and allergens promote epithelial damage and trigger the generation of IL-25, IL-33, and TSLP via innate pathways such as TLRs and purinergic receptors. Similarly, engineered nanomaterials promote a Th2-associated pathophysiology. In this study, we tested the hypothesis that instillation of multi-walled carbon nanotubes (MWCNT) impair pulmonary function in C57Bl/6 mice due to the development of IL-33-dependent Th2-associated inflammation. MWCNT exposure resulted in elevated levels of IL-33 in the lavage fluid (likely originating from airway epithelial cells), enhanced AHR, eosinophil recruitment, and production of Th2-associated cytokines and chemokines. Moreover, these events were dependent on IL-13 signaling and the IL-33/ST2 axis, but independent of T and B cells. Finally, MWCNT exposure resulted in the recruitment of innate lymphoid cells. Collectively, our data suggest that MWCNT induce epithelial damage that results in release of IL-33, which in turn promotes innate lymphoid cell recruitment and the development of IL-13-dependent inflammatory response.
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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.