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Protocols to Evaluate Cigarette Smoke-Induced Lung Inflammation and Pathology in Mice

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Inflammation and Cancer

Part of the book series: Methods in Molecular Biology ((MIMB,volume 1725))

Abstract

Cigarette smoking is a major cause of chronic obstructive pulmonary disease (COPD). Inhalation of cigarette smoke causes inflammation of the airways, airway wall remodelling, mucus hypersecretion and progressive airflow limitation. Much of the disease burden and health care utilisation in COPD is associated with the management of its comorbidities and infectious (viral and bacterial) exacerbations (AECOPD). Comorbidities, in particular skeletal muscle wasting, cardiovascular disease and lung cancer markedly impact on disease morbidity, progression and mortality. The mechanisms and mediators underlying COPD and its comorbidities are poorly understood and current COPD therapy is relatively ineffective. Many researchers 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 describe a mouse model that we have developed to define the cellular, molecular and pathological consequences of cigarette smoke exposure and the development of comorbidities of COPD.

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Acknowledgement

This work was supported by NHMRC Project Grants 1084627 and 1067547.

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Correspondence to Ross Vlahos .

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Vlahos, R., Bozinovski, S. (2018). Protocols to Evaluate Cigarette Smoke-Induced Lung Inflammation and Pathology in Mice. In: Jenkins, B. (eds) Inflammation and Cancer. Methods in Molecular Biology, vol 1725. Humana Press, New York, NY. https://doi.org/10.1007/978-1-4939-7568-6_5

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  • DOI: https://doi.org/10.1007/978-1-4939-7568-6_5

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  • Publisher Name: Humana Press, New York, NY

  • Print ISBN: 978-1-4939-7567-9

  • Online ISBN: 978-1-4939-7568-6

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