ArticleAmerican journal of respiratory cell and molecular biology2015
Role of signal transducer and activator of transcription 1 in murine allergen-induced airway remodeling and exacerbation by carbon nanotubes.
Article in American journal of respiratory cell and molecular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 42 citations in OpenAlex.
- Role of the protease-activated receptor 2 in multi-walled carbon nanotube-induced macrophage polarizationFrontiers in toxicology · 2026Article
- Identification of common genes of rhinovirus single/double‑stranded RNA‑induced asthma deterioration by bioinformatics analysis.Experimental and therapeutic medicine · 2024Article
- Role of the protease-activated receptor-2 (PAR2) in the exacerbation of house dust mite-induced murine allergic lung disease by multi-walled carbon nanotubes.Particle and fibre toxicology · 2023Article
- Nanoparticles-induced potential toxicity on human health: Applications, toxicity mechanisms, and evaluation models.MedComm · 2023Review
- Toxicity and Mechanisms of Engineered Nanoparticles in Animals with Established Allergic Asthma.International journal of nanomedicine · 2023Review
- Eosinophil extracellular traps drive asthma progression through neuro-immune signals.Nature cell biology · 2021Article
- STAT6-Dependent Exacerbation of House Dust Mite-Induced Allergic Airway Disease in Mice by Multi-Walled Carbon Nanotubes.NanoImpact · 2021Article
- The pulmonary toxicity of carboxylated or aminated multi-walled carbon nanotubes in mice is determined by the prior purification method.Particle and fibre toxicology · 2020Article
- Susceptibility Factors in Chronic Lung Inflammatory Responses to Engineered Nanomaterials.International journal of molecular sciences · 2020Review
- Sex differences in the acute and subchronic lung inflammatory responses of mice to nickel nanoparticles.Nanotoxicology · 2020Article
- Integration of inflammation, fibrosis, and cancer induced by carbon nanotubes.Nanotoxicology · 2019Review
- Article
- Mechanisms of carbon nanotube-induced pulmonary fibrosis: a physicochemical characteristic perspective.Wiley interdisciplinary reviews. Nanomedicine and nanobiotechnology · 2018Review
- The Toxicology of Engineered Nanomaterials in Asthma.Current environmental health reports · 2018Review
- Mechanistic insight into the impact of nanomaterials on asthma and allergic airway disease.Particle and fibre toxicology · 2017Review
- Stat-6 signaling pathway and not Interleukin-1 mediates multi-walled carbon nanotube-induced lung fibrosis in mice: insights from an adverse outcome pathway framework.Particle and fibre toxicology · 2017Article
- STAT1-dependent and -independent pulmonary allergic and fibrogenic responses in mice after exposure to tangled versus rod-like multi-walled carbon nanotubes.Particle and fibre toxicology · 2017Article
- Increased antioxidant activity after exposure of ozone in murine asthma model.Asia Pacific allergy · 2017Article
- Osteopontin enhances multi-walled carbon nanotube-triggered lung fibrosis by promoting TGF-β1 activation and myofibroblast differentiation.Particle and fibre toxicology · 2017Article
- Impacts of meteorological and environmental factors on allergic rhinitis in children.International journal of biometeorology · 2017Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Asthma is characterized by a T helper type 2 phenotype and by chronic allergen-induced airway inflammation (AAI). Environmental exposure to air pollution ultrafine particles (i.e., nanoparticles) exacerbates AAI, and a concern is possible exacerbation posed by engineered nanoparticles generated by emerging nanotechnologies. Signal transducer and activator of transcription (STAT) 1 is a transcription factor that maintains T helper type 1 cell development. However, the role of STAT1 in regulating AAI or exacerbation by nanoparticles has not been explored. In this study, mice with whole-body knockout of the Stat1 gene (Stat1(-/-)) or wild-type (WT) mice were sensitized to ovalbumin (OVA) allergen and then exposed to multiwalled carbon nanotubes (MWCNTs) by oropharygneal aspiration. In Stat1(-/-) and WT mice, OVA increased eosinophils in bronchoalveolar lavage fluid, whereas MWCNTs increased neutrophils. Interestingly, OVA sensitization prevented MWCNT-induced neutrophilia and caused only eosinophilic inflammation. Stat1(-/-) mice displayed increased IL-13 in bronchoalveolar lavage fluid at 1 day compared with WT mice after treatment with OVA or OVA and MWCNTs. At 21 days, the lungs of OVA-sensitized Stat1(-/-) mice displayed increased eosinophilia, goblet cell hyperplasia, airway fibrosis, and subepithelial apoptosis. MWCNTs further increased OVA-induced goblet cell hyperplasia, airway fibrosis, and apoptosis in Stat1(-/-) mice at 21 days. These changes corresponded to increased levels of profibrogenic mediators (transforming growth factor-β1, TNF-α, osteopontin) but decreased IL-10 in Stat1(-/-) mice. Finally, fibroblasts isolated from the lungs of Stat1(-/-) mice produced significantly more collagen mRNA and protein in response to transforming growth factor-β1 compared with WT lung fibroblasts. Our results support a protective role for STAT1 in chronic AAI and exacerbation of remodeling caused by MWCNTs.
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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.