Chronic Obstructive Pulmonary Disease
Chronic obstructive pulmonary disease (COPD) is a term used to refer to a set of chronic lung diseases with pulmonary manifestations (e.g. emphysema, chronic bronchitis, or a combination of both) resulting from exposure to inhaled irritants such as cigarette smoke and environmental pollutants. The pulmonary aspects of COPD typically include characteristic lesions, chronic inflammation, excessive mucus production, and a degree of fixed airflow limitation associated with disease severity. This disease is one of the major causes of morbidity and mortality worldwide. In the clinical setting, physicians rely heavily on spirometry and its outcome parameters (e.g. FEV1 and FVC) for diagnosis and monitoring as well as for the assessment of disease severity, as defined by the GOLD scale. Other lung function measurements, such as pressure-volume curves, forced oscillations, or thoracic imaging, are used in addition to bronchoprovocation tests to establish a diagnosis or evaluate disease progression.
COMPREHENSIVE AND INTEGRATED ASSESSMENT
In preclinical research, the challenge is often to link structural changes (e.g. cigarette-smoke induced alveolar destruction) to altered lung function measurements, such as resistance, compliance or spirometry outcomes. The flexiVent is a comprehensive tool allowing an integrated assessment of various disease determinants (e.g. extent and pattern of induced damage) on lung function decline. It measures the mechanical properties of the lungs with high sensitivity and reproducibility. In addition, it reliably evaluates COPD-diseased lungs through pressure-volume curves, changes in lung volume (e.g. inspiratory or forced vital capacities), or forced expiration outcomes, providing clinically relevant information.
- HIV infection model of chronic obstructive pulmonary disease in mice – Geraghty, P. et al. American journal of physiology. Lung cellular and molecular physiology. 312(4), pp. L500–L509. 2017.
- Chronic exposure to electronic cigarettes results in impaired cardiovascular function in mice – Olfert, I. M. et al. Journal of Applied Physiology. American Physiological Society Bethesda, MD , 124(3), pp. 573–582. 2018.
- Subcutaneous administration of neutralizing antibodies to endothelial monocyte-activating protein II attenuates cigarette smoke-induced lung injury in mice – Koike, K. et al. American Journal of Physiology-Lung Cellular and Molecular Physiology. 316(3), pp. L558–L566. 2019.
- Elimination of p19 ARF -expressing cells protects against pulmonary emphysema in mice – Mikawa, R., et al. Aging Cell, 17(5). 2018.
- A critical role for ABC transporters in persistent lung inflammation in the development of emphysema after smoke exposure – Sonett, J., et al. FASEB Journal, 32(12), 6724–6736. 2018.
COMPACT, REPRODUCIBLE, AUTOMATED
The inExpose is a compact, computer controlled system and can integrate with several smoke generation devices and adapters to suit a wide range of specific smoke applications. Its low internal volume allows desired concentrations to be reached with minimal tobacco quantities. The pumps are specifically designed to deliver standard and customized puff profiles. Industry standards such as the commonly used ISO standard or the Massachusetts or Canadian profiles are often used to generate COPD models.
Smoke composition will be influenced by a number of technical factors. For example, the constituents of smoke will differ whether the smoke is drawn from side-stream, main-stream, or environmental tobacco smoke. Different brands of cigarettes, water filtered smoke (hookah), cigars, or other tobacco smoke preparations will result in different compositions. In addition, the choice of the puff profile will influence cigarette yields. It is therefore important, when studying the impacts of tobacco smoke, to consistently and reproducibly be able to introduce the same smoke composition at each experimental session.
To date, this versatility and programmability of the inExpose system has been employed in a variety of exposure studies, both in vivo and in vitro, to evaluate the effects of smoke.
- SCIREQ Application Note: Reproducible Respiratory Research.
- Smoke-induced neuromuscular junction degeneration precedes the fibre type shift and atrophy in chronic obstructive pulmonary disease. Kapchinsky, S., et al. Journal of Physiology, 596(14), 2865–2881. 2018.
- A ferret model of COPD-related chronic bronchitis. Raju, S. V., et al. JCI Insight, 1(15). 2016.
- Airway bacteria drive a progressive COPD-like phenotype in mice with polymeric immunoglobulin receptor deficiency. Richmond, B. W., et al. Nature Communications, 7. 2016.
- Airway infection with Nontypeable Haemophilus influenzae is more rapidly eradicated in vitamin D deficient mice. Serré, J., et al. Journal of Steroid Biochemistry and Molecular Biology, 187(October), 42–51. 2019.
- Involvement of Lamin B1 Reduction in Accelerated Cellular Senescence during Chronic Obstructive Pulmonary Disease Pathogenesis. Saito, N., et al. The Journal of Immunology, 202(5), 1428–1440. 2019.
- Bacterial-derived neutrophilic inflammation drives lung remodeling in a mouse model of chronic obstructive pulmonary disease. Richmond, B. W., et al. American Journal of Respiratory Cell and Molecular Biology, 58(6), 736–744. 2018.
Symptoms of COPD include dyspnea, chronic cough, and chronic sputum production. Plethysmography, as a non-invasive technique, offers a powerful means of rapidly screening subjects based on changes in ventilatory parameters (e.g. breathing frequency, tidal volume, peak inspiratory or expiratory flows). Events such as coughing can also be detected and monitored.
- Effects of cigarette smoke and chronic hypoxia on airways remodeling and resistance. Clinical significance. – Olea et al. Respir Physiol Neurobiol., 15;179(2-3):305-13, 2011.
- Extracellular matrix defects in aneurysmal Fibulin-4 mice predispose to lung emphysema. – Ramnath et al. PLOS ONe, 9(9):e106054, 2014.
- Use of cyclodextrin for treatment and prevention of bronchial inflammatory diseases. – Cataldo, Didier. Patent application US 13/804,626.
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