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Assessing Lung Inflammation and Pathology in Preclinical Models of Chronic Obstructive Pulmonary Disease
Ross Vlahos1, Hao Wang2, Steven Bozinovski2
1Centre for Respiratory Science and Health, School of Health and Biomedical Sciences, RMIT University, Bundoora, VIC, Australia. ross.vlahos@rmit.edu.au.
Abstract:
Chronic obstructive pulmonary disease (COPD) is an incurable disease that is a major cause of mortality and morbidity worldwide. Cigarette smoking is a major cause of COPD and triggers progressive airflow limitation, chronic lung inflammation, and irreversible lung damage and decline in lung function. COPD patients often experience various extrapulmonary comorbid diseases, including cardiovascular disease, skeletal muscle wasting, lung cancer, and cognitive decline which markedly impact on disease morbidity, progression, and mortality. People with COPD are also susceptible to respiratory infections which cause exacerbations of the underlying disease (AECOPD). The mechanisms and mediators underlying COPD and its comorbidities are poorly understood and current COPD therapy is relatively ineffective. We and others have used animal modelling systems to explore the mechanisms underlying COPD, AECOPD, and comorbidities of COPD with the goal of identifying novel therapeutic targets. Here we provide a preclinical model and protocols to assess the cellular, molecular, and pathological consequences of cigarette smoke exposure and the development of comorbidities of COPD.
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