Literature DB >> 29322408

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

Ross Vlahos1, Steven Bozinovski2.   

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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Keywords:  AECOPD; COPD; Cigarette smoke; Comorbidities; Emphysema; Lung inflammation

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Year:  2018        PMID: 29322408     DOI: 10.1007/978-1-4939-7568-6_5

Source DB:  PubMed          Journal:  Methods Mol Biol        ISSN: 1064-3745


  1 in total

1.  An innate contribution of human nicotinic receptor polymorphisms to COPD-like lesions.

Authors:  Philippe Birembaut; Valérian Dormoy; Uwe Maskos; Julie Routhier; Stéphanie Pons; Mohamed Lamine Freidja; Véronique Dalstein; Jérôme Cutrona; Antoine Jonquet; Nathalie Lalun; Jean-Claude Mérol; Mark Lathrop; Jerry A Stitzel; Gwenola Kervoaze; Muriel Pichavant; Philippe Gosset; Jean-Marie Tournier
Journal:  Nat Commun       Date:  2021-11-04       Impact factor: 14.919

  1 in total

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