ArticleAmerican journal of respiratory cell and molecular biology2011
Novel murine model of chronic granulomatous lung inflammation elicited by carbon nanotubes.
Article in American journal of respiratory cell and molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 93 citations in OpenAlex.
- Review
- Review
- Coccidioidomycosis Granulomas Informed by Other Diseases: Advancements, Gaps, and Challenges.Journal of fungi (Basel, Switzerland) · 2023Review
- Sarcoidosis and Autoimmune Inflammatory Syndrome Induced by Adjuvants.Life (Basel, Switzerland) · 2023Review
- Innate but Not Adaptive Immunity Regulates Lung Recovery from Chronic Exposure to Graphene Oxide Nanosheets.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Pharmacological Inhibition of Chitotriosidase (CHIT1) as a Novel Therapeutic Approach for Sarcoidosis.Journal of inflammation research · 2022Article
- Systemic immune response to vimentin and granuloma formation in a model of pulmonary sarcoidosis.Journal of translational autoimmunity · 2022Article
- Myeloid ABCG1 Deficiency Enhances Apoptosis and Initiates Efferocytosis in Bronchoalveolar Lavage Cells of Murine Multi-Walled Carbon Nanotube-Induced Granuloma Model.International journal of molecular sciences · 2021Article
- The M2a Macrophage Phenotype Accompanies Pulmonary Granuloma Resolution inInternational journal of molecular sciences · 2021Article
- Osteopontin mRNA expression by rat mesothelial cells exposed to multi-walled carbon nanotubes as a potential biomarker of chronic neoplastic transformation in vitro.Toxicology in vitro : an international journal published in association with BIBRA · 2021Article
- 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
- SOX2Mediates Carbon Nanotube-Induced Fibrogenesis and Fibroblast Stem Cell Acquisition.ACS biomaterials science & engineering · 2020Article
- Models Contribution to the Understanding of Sarcoidosis Pathogenesis: "Are There Good Models of Sarcoidosis?"Journal of clinical medicine · 2020Review
- Size-Dependent Pulmonary Impact of Thin Graphene Oxide Sheets in Mice: Toward Safe-by-Design.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Article
- Microenvironmental Alterations in Carbon Nanotube-Induced Lung Inflammation and Fibrosis.Frontiers in cell and developmental biology · 2020Review
- Matrix Metalloproteinase-12 Is Required for Granuloma Progression.Frontiers in immunology · 2020Article
- Current Sarcoidosis Models and the Importance of Focusing on the Granuloma.Frontiers in immunology · 2020Review
- PPARγ Deficiency in Carbon Nanotube-elicited Granulomatous Inflammation Promotes a Th17 Response to a Microbial Antigen.Journal of nanomedicine & nanotechnology · 2020Article
- Integration of inflammation, fibrosis, and cancer induced by carbon nanotubes.Nanotoxicology · 2019Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
Abstract
Lung granulomas are associated with numerous conditions, including inflammatory disorders, exposure to environmental pollutants, and infection. Osteopontin is a chemotactic cytokine produced by macrophages, and is implicated in extracellular matrix remodeling. Furthermore, osteopontin is up-regulated in granulomatous disease, and osteopontin null mice exhibit reduced granuloma formation. Animal models currently used to investigate chronic lung granulomatous inflammation bear a pathological resemblance, but lack the chronic nature of human granulomatous disease. Carbon nanoparticles are generated as byproducts of combustion. Interestingly, experimental exposures to carbon nanoparticles induce pulmonary granuloma-like lesions. However, the recruited cellular populations and extracellular matrix gene expression profiles within these lesions have not been explored. Because of the rapid resolution of granulomas in current animal models, the mechanisms responsible for persistence have been elusive. To overcome the limitations of previous models, we investigated whether a model using multiwall carbon nanoparticles would resemble chronic human lung granulomatous inflammation. We hypothesized that pulmonary exposure to multiwall carbon nanoparticles would induce granulomas, elicit a macrophage and T-cell response, and mimic other granulomatous disorders with an up-regulation of osteopontin. This model demonstrates: (1) granulomatous inflammation, with macrophage and T-cell infiltration; (2) resemblance to the chronicity of human granulomas, with persistence up to 90 days; and (3) a marked elevation of osteopontin, metalloproteinases, and cell adhesion molecules in granulomatous foci isolated by laser-capture microdissection and in alveolar macrophages from bronchoalveolar lavage. The establishment of such a model provides an important platform for mechanistic studies on the persistence of granuloma.
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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.