ArticleParticle and fibre toxicology2014
Nickel nanoparticles cause exaggerated lung and airway remodeling in mice lacking the T-box transcription factor, TBX21 (T-bet).
Article in Particle and fibre toxicology, 2014. 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, 49 citations in OpenAlex.
- The pulmonary effects of nickel-containing nanoparticles: Cytotoxicity, genotoxicity, carcinogenicity, and their underlying mechanisms.Environmental science. Nano · 2024Article
- Comparison of preventive and therapeutic effects of continuous exercise on acute lung injury induced with methotrexate.Experimental physiology · 2023Article
- Nickel oxide nanoparticles exposure as a risk factor for male infertility: "Frontiers in endocrinology · 2023Article
- Role of Macrophages in Air Pollution Exposure Related Asthma.International journal of molecular sciences · 2022Review
- Concepts of advanced therapeutic delivery systems for the management of remodeling and inflammation in airway diseases.Future medicinal chemistry · 2022Review
- miR-21 mediates nickel nanoparticle-induced pulmonary injury and fibrosis.Nanotoxicology · 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
- Advance on toxicity of metal nickel nanoparticles.Environmental geochemistry and health · 2020Review
- Study on the damage of sperm induced by nickel nanoparticle exposure.Environmental geochemistry and health · 2020Article
- Metal nanomaterials: Immune effects and implications of physicochemical properties on sensitization, elicitation, and exacerbation of allergic disease.Journal of immunotoxicology · 2019Review
- Surface area- and mass-based comparison of fine and ultrafine nickel oxide lung toxicity and augmentation of allergic response in an ovalbumin asthma model.Inhalation toxicology · 2019Article
- Comparative mouse lung injury by nickel nanoparticles with differential surface modification.Journal of nanobiotechnology · 2019Article
- Accelerated inflammation and oxidative stress induced by LPS in acute lung injury: Ιnhibition by ST1926.International journal of molecular medicine · 2018Article
- 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
- Synthetic Nanoparticles That Promote Tumor Necrosis Factor Receptor 2 Expressing Regulatory T Cells in the Lung and Resistance to Allergic Airways Inflammation.Frontiers in immunology · 2017Article
- Biomarkers of susceptibility: State of the art and implications for occupational exposure to engineered nanomaterials.Toxicology and applied pharmacology · 2016Review
- Extracellular HMGB1 regulates multi-walled carbon nanotube-induced inflammation in vivo.Nanotoxicology · 2015Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundNickel nanoparticles (NiNPs) are increasingly used in a variety of industrial applications, including the manufacturing of multi-walled carbon nanotubes (MWCNTs). While occupational nickel exposure is a known cause of pulmonary alveolitis, fibrosis, and cancer, the health risks of NiNPs are not well understood, especially in susceptible individuals such as asthmatics. The T-box transcription factor Tbx21 (T-bet) maintains Th1 cell development and loss of T-bet is associated with a shift towards Th2 type allergic airway inflammation that characterizes asthma. The purpose of this study was to determine the role of T-bet in susceptibility to lung remodeling by NiNPs or MWCNTs.
methodsWild-type (WT) and T-bet-/- mice were exposed to NiNPs or MWCNTs (4 mg/kg) by oropharyngeal aspiration (OPA). Necropsy was performed at 1 and 21 days. Bronchoalveolar lavage fluid (BALF) was collected for differential counting of inflammatory cells and for measurement of cytokines by ELISA. The left lung was collected for histopathology. The right lung was analyzed for cytokine or mucin (MUC5AC and MUC5B) mRNAs.
resultsMorphometry of alcian-blue/periodic acid Schiff (AB/PAS)-stained lung tissue showed that NiNPs significantly increased mucous cell metaplasia in T-bet-/- mice at 21 days (p < 0.001) compared to WT mice, and increased MUC5AC and MUC5B mRNAs (p < 0.05). MWCNTs also increased mucous cell metaplasia in T-bet-/- mice, but to a lesser extent than NiNPs. Chronic alveolitis was also increased by NiNPs, but not MWCNTs, in T-bet-/- mice compared to WT mice at 21 days (P < 0.001). NiNPs also increased IL-13 and eosinophils (p < 0.001) in BALF from T-bet-/- mice after 1 day. Interestingly, the chemokine CCL2 in the BALF of T-bet-/- mice was increased at 1 and 21 days (p < 0.001 and p < 0.05, respectively) by NiNPs, and to a lesser extent by MWCNTs at 1 day. Treatment of T-bet-/- mice with a monoclonal anti-CCL2 antibody enhanced NiNP-induced mucous cell metaplasia and MUC5AC mRNA levels (p < 0.05), yet marginally reduced NiNP-induced alveolitis.
conclusionThese findings identify T-bet as a potentially important susceptibility factor for NiNP exposure and to a lesser extent for MWCNT exposure, and suggests that individuals with asthma are at greater risk.
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