ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015
Experimental progressive emphysema in BALB/cJ mice as a model for chronic alveolar destruction in humans.
Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 47 citations in OpenAlex.
- Molecular and Cellular Mechanisms Responsible for Beneficial Effects of Mesenchymal Stem Cell-Derived Product "Exo-d-MAPPS" in Attenuation of Chronic Airway Inflammation.Analytical cellular pathology (Amsterdam) · 2020Trial
- Preclinical models of COPD: a state of the art review.The European respiratory journal · 2026Review
- Feasibility of longitudinal in vivo monitoring of pulmonary disease progression in mouse models using laboratory-based x-ray dark-field CT.European radiology experimental · 2026Article
- UBE2M deficiency in alveolar macrophages promotes emphysema through HIF-2α/MMP12 axis.Chinese medical journal pulmonary and critical care medicine · 2026Article
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- Hyaluronic acid synthase 2 dysfunction exacerbates elastase-induced neutrophilic airway inflammation and emphysema in mice.Frontiers in immunology · 2025Article
- D-cycloserine effects on COPD and depression in a murine experimental model.Frontiers in pharmacology · 2025Article
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- Decreased fucosylation impacts epithelial integrity and increases risk for COPD.bioRxiv : the preprint server for biology · 2023Article
- Fibroblast growth factor 10 reverses cigarette smoke- and elastase-induced emphysema and pulmonary hypertension in mice.The European respiratory journal · 2023Article
- Lung stiffness of C57BL/6 versus BALB/c mice.Scientific reports · 2023Article
- Article
- Lung microhaemorrhage drives oxidative/inflammatory damage in αERJ open research · 2023Article
- Loss of E-cadherin is causal to pathologic changes in chronic lung disease.Communications biology · 2022Article
- Protocol for assessing senescence-associated lung pathologies in mice.STAR protocols · 2021Article
- Therapeutic benefits of recombinant alpha1-antitrypsin IgG1 Fc-fusion protein in experimental emphysema.Respiratory research · 2021Article
- Airway compliance measurements in mouse models of respiratory diseases.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Dual interleukin-17A/F deficiency protects against acute and chronic response to cigarette smoke exposure in mice.Scientific reports · 2021Article
- Oscillometry of the respiratory system: a translational opportunity not to be missed.American journal of physiology. Lung cellular and molecular physiology · 2021Review
- Effect of an Adenovirus-Vectored Universal Influenza Virus Vaccine on Pulmonary Pathophysiology in a Mouse Model.Journal of virology · 2021Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Emphysema, one of the major components of chronic obstructive pulmonary disease (COPD), is characterized by the progressive and irreversible loss of alveolar lung tissue. Even though >80% of COPD cases are associated with cigarette smoking, only a relatively small proportion of smokers develop emphysema, suggesting a potential role for genetic factors in determining individual susceptibility to emphysema. Although strain-dependent effects have been shown in animal models of emphysema, the molecular basis underlying this intrinsic susceptibility is not fully understood. In this present study, we investigated emphysema development using the elastase-induced experimental emphysema model in two commonly used mouse strains, C57BL/6J and BALB/cJ. The results demonstrate that mice with different genetic backgrounds show disparate susceptibility to the development of emphysema. BALB/cJ mice were found to be much more sensitive than C57BL/6J to elastase injury in both a dose-dependent and time-dependent manner, as measured by significantly higher mortality, greater body weight loss, greater decline in lung function, and a greater loss of alveolar tissue. The more susceptible BALB/cJ strain also showed the persistence of inflammatory cells in the lung, especially macrophages and lymphocytes. A comparative gene expression analysis following elastase-induced injury showed BALB/cJ mice had elevated levels of il17A mRNA and a number of classically (M1) and alternatively (M2) activated macrophage genes, whereas the C57BL/6J mice demonstrated augmented levels of interferon-γ. These findings suggest a possible role for these cellular and molecular mediators in modulating the severity of emphysema and highlight the possibility that they might contribute to the heterogeneity observed in clinical emphysema outcomes.
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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.