Abstract
Animal model of cigarette smoke (CS) –induced chronic obstructive pulmonary disease (COPD) is the primary testing methodology for drug therapies and studies on pathogenic mechanisms of disease. However, researchers have rarely run simultaneous or side-by-side tests of whole-body and nose-only CS exposure in building their mouse models of COPD. We compared and evaluated these two different methods of CS exposure, plus airway Lipopolysaccharides (LPS) inhalation, in building our COPD mouse model. Compared with the control group, CS exposed mice showed significant increased inspiratory resistance, functional residual capacity, right ventricular hypertrophy index, and total cell count in BALF. Moreover, histological staining exhibited goblet cell hyperplasia, lung inflammation, thickening of smooth muscle layer on bronchia, and lung angiogenesis in both methods of CS exposure. Our data indicated that a viable mouse model of COPD can be established by combining the results from whole-body CS exposure, nose-only CS exposure, and airway LPS inhalation testing. However, in our study, we also found that, given the same amount of particulate intake, changes in right ventricular pressure and intimal thickening of pulmonary small artery are a little more serious in nose-only CS exposure method than changes in the whole-body CS exposure method.
Highlights
Chronic Obstructive Pulmonary Disease (COPD), a common preventable and treatable disease, is characterized by persistent airflow limitation, is usually progressive, and is associated with an enhanced chronic inflammatory response to noxious particles or gases in the airways and the lung
Cigarette smoke (CS) exposure and whole-body CS exposure caused a significant increase in FRC (P < 0.01), C-chord (P < 0.01), inspiratory resistance (P < 0.01), and caused a decrease in FEV50/forced vital capacity (FVC) (P < 0.01) and Forced expiration volume in 100 milliseconds (FEV100)/FVC (P < 0.01)
The data from our study provides evidence that both the nose-only CS exposure, and the whole-body CS exposure, adding airway LPS inhalation to each, can induce chronic airway inflammation, lung function impairment, emphysema, and right ventricular dysfunction, which are all important disease processes to have present for study, in order to create a complete mouse model
Summary
Chronic Obstructive Pulmonary Disease (COPD), a common preventable and treatable disease, is characterized by persistent airflow limitation, is usually progressive, and is associated with an enhanced chronic inflammatory response to noxious particles or gases in the airways and the lung. COPD morbidity and mortality are significantly increased by the common occurrence of pulmonary hypertension associated with cigarette smoke[5]. Sun[11] established a COPD rat model which well recapitulates the pathophysiology and development of human COPD, by implementing a method which combines cigarette smoke exposure and trachea injection of LPS, to simulate smoking and infection, two most important incentives to developing human COPD. This combination of LPS and CS aimed to simulate the acute exacerbation of COPD symptoms seen in patients with infection, who suffer a sharp decline in pulmonary function
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