Vlahos Ross, Bozinovski Steven
School of Health and Biomedical Sciences, RMIT University, Bundoora, VIC, Australia.
Methods Mol Biol. 2018;1725:53-63. doi: 10.1007/978-1-4939-7568-6_5.
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.
吸烟是慢性阻塞性肺疾病（COPD）的主要病因。吸入香烟烟雾会导致气道炎症、气道壁重塑、黏液分泌过多以及进行性气流受限。COPD的许多疾病负担和医疗保健利用都与其合并症的管理以及感染性（病毒和细菌）加重（慢性阻塞性肺疾病急性加重，AECOPD）有关。合并症，尤其是骨骼肌消瘦、心血管疾病和肺癌，对疾病的发病率、进展和死亡率有显著影响。COPD及其合并症的潜在机制和介质了解甚少，目前的COPD治疗相对无效。许多研究人员使用动物模型系统来探索COPD、AECOPD以及COPD合并症的潜在机制，目的是确定新的治疗靶点。在此，我们描述一种我们开发的小鼠模型，以确定香烟烟雾暴露的细胞、分子和病理后果以及COPD合并症的发展情况。
