ArticleJournal of nanomedicine & nanotechnology2015
Exposure to a Mycobacterial Antigen, ESAT-6, Exacerbates Granulomatous and Fibrotic Changes in a Multiwall Carbon Nanotube Model of Chronic Pulmonary Disease.
Article in Journal of nanomedicine & nanotechnology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- Quercetin improves ESAT-6-induced pleural mesothelial cell fibrosis by activating the Nrf2/HO-1 pathway.Iranian journal of basic medical sciences · 2026Article
- The Toxicological Profile of Active Pharmaceutical Ingredients-Containing Nanoparticles: Classification, Mechanistic Pathways, and Health Implications.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Pulmonary Sarcoidosis: Experimental Models and Perspectives of Molecular Diagnostics Using Quantum Dots.International journal of molecular sciences · 2023Review
- Pharmacological Inhibition of Chitotriosidase (CHIT1) as a Novel Therapeutic Approach for Sarcoidosis.Journal of inflammation research · 2022Article
- Studies in a Murine Granuloma Model of Instilled Carbon Nanotubes: Relevance to Sarcoidosis.International journal of molecular sciences · 2021Review
- Impaired mitochondrial function of alveolar macrophages in carbon nanotube-induced chronic pulmonary granulomatous disease.Toxicology · 2020Article
- Models Contribution to the Understanding of Sarcoidosis Pathogenesis: "Are There Good Models of Sarcoidosis?"Journal of clinical medicine · 2020Review
- PPARγ Deficiency in Carbon Nanotube-elicited Granulomatous Inflammation Promotes a Th17 Response to a Microbial Antigen.Journal of nanomedicine & nanotechnology · 2020Article
- Matrix Metalloproteinase-12 Is Required for Granuloma Progression.Frontiers in immunology · 2020Article
- Alveolar Macrophage ABCG1 Deficiency Promotes Pulmonary Granulomatous Inflammation.American journal of respiratory cell and molecular biology · 2019Article
- Peroxisome Proliferator-activated Receptor-γ Deficiency Exacerbates Fibrotic Response to Mycobacteria Peptide in Murine Sarcoidosis Model.American journal of respiratory cell and molecular biology · 2019Article
- Article
- Transcriptional survey of alveolar macrophages in a murine model of chronic granulomatous inflammation reveals common themes with human sarcoidosis.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Type 2 Immune Mechanisms in Carbon Nanotube-Induced Lung Fibrosis.Frontiers in immunology · 2018Review
- Osteopontin enhances multi-walled carbon nanotube-triggered lung fibrosis by promoting TGF-β1 activation and myofibroblast differentiation.Particle and fibre toxicology · 2017Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Recent studies suggest additive effects of environmental pollutants and microbial antigens on respiratory disease. We established a granuloma model in which instilled multiwall carbon nanotubes (MWCNT) elicit granulomatous pathology. We hypothesized that mycobacterial antigen ESAT-6, a T cell activator associated with tuberculosis and sarcoidosis, might alter pathology. Wild-type C57Bl/6 mice received MWCNT with or without ESAT-6 peptide. Controls received vehicle (surfactant-PBS) or ESAT-6 alone. Mice were evaluated 60 days later for granulomas, fibrosis, and bronchoalveolar lavage (BAL) cell expression of inflammatory mediators (CCL2, MMP-12, and Osteopontin). Results indicated increased granulomas, fibrosis, and inflammatory mediators in mice receiving the combination of MWCNT+ESAT-6 compared to MWCNT or vehicle alone. ESAT-6 alone showed no significant effect on these pathological endpoints. However, CD3 (+) lymphocyte infiltration of lung tissue increased with MWCNT+ESAT-6 versus MWCNT alone. Findings suggest that concurrent exposure to microbial antigen and MWCNT exacerbates chronic pulmonary disease.
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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.