Dynamic evolution of emphysema and airway remodeling in two mouse models of COPD

Yue Yang,Congli Fu,Tao Bian,Zixiao Zhang,Yan Wu,Tingting Di,Jiaxin Liu

doi:10.1186/s12890-021-01456-z

Yue Yang, Congli Fu + Show 5 more

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https://doi.org/10.1186/s12890-021-01456-z

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Abstract

BackgroundEstablishment of a mouse model is important for investigating the mechanism of chronic obstructive pulmonary disease (COPD). In this study, we observed and compared the evolution of the pathology in two mouse models of COPD induced by cigarette smoke (CS) exposure alone or in combination with lipopolysaccharide (LPS).MethodsOne hundred eight wild-type C57BL/6 mice were equally divided into three groups: the (1) control group, (2) CS-exposed group (CS group), and (3) CS + LPS-exposed group (CS + LPS group). The body weight of the mice was recorded, and noninvasive lung function tests were performed monthly. Inflammation was evaluated by counting the number of inflammatory cells in bronchoalveolar lavage fluid and measuring the expression of the IL-6 mRNA in mouse lung tissue. Changes in pathology were assessed by performing hematoxylin and eosin and Masson staining of lung tissue sections.ResultsThe two treatments induced emphysema and airway remodeling and decreased lung function. Emphysema was induced after 1 month of exposure to CS or CS + LPS, while airway remodeling was induced after 2 months of exposure to CS + LPS and 3 months of exposure to CS. Moreover, the mice in the CS + LPS group exhibited more severe inflammation and airway remodeling than the mice in the CS group, but the two treatments induced similar levels of emphysema.ConclusionCompared with the single CS exposure method, the CS + LPS exposure method is a more suitable model of COPD in airway remodeling research. Conversely, the CS exposure method is a more suitable model of COPD for emphysema research due to its simple operation.

Highlights

Chronic obstructive pulmonary disease (COPD) is a chronic progressive lung disease characterized by a persistently limited airflow, chronic airway inflammation, Yang et al BMC Pulm Med (2021) 21:134Mice are always suitable animals to establish chronic obstructive pulmonary disease (COPD) models due to their genetic similarity to humans, ease of breeding, high survival rate and extensive study [5, 6]
Mice in the cigarette smoke (CS) + LPS group presented a lower body weight than mice in the CS group During CS or CS + LPS exposure, the body weights of mice in both the CS group and CS + LPS group were lower than mice in the control group (P < 0.01), and the lowest body weights were recorded in the CS + LPS group (P < 0.05) (Fig. 4a)
Greater amounts of collagen deposition were observed in the airways of the CS + LPS group than in the CS group In the present study, Masson’s trichrome staining of lungs from both the CS and CS + LPS groups showed collagen deposition, airway thickening and inflammatory cell 6 months or CS for 6 months and an intranasal instillation of LPS on days 1 and 14. a Trends in the body weights of mice in the control group (n = 6), CS group (n = 6) and CS + LPS group (n = 6). b Lung function of mice in the control group (n = 6), CS group (n = 6) and CS + LPS group (n = 6)

Summary

Introduction

Chronic obstructive pulmonary disease (COPD) is a chronic progressive lung disease characterized by a persistently limited airflow, chronic airway inflammation, Yang et al BMC Pulm Med (2021) 21:134Mice are always suitable animals to establish COPD models due to their genetic similarity to humans, ease of breeding, high survival rate and extensive study [5, 6]. Because exposure to cigarette smoke (CS) is an independent risk factor for COPD [7, 8], long-term CS exposure is one of the widely accepted methods for modeling COPD [9,10,11]. We first evaluated and compared the dynamic evolution of the pathology and lung function in these two most widely used mouse models of COPD to provide evidence for further COPD modelling. Establishment of a mouse model is important for investigating the mechanism of chronic obstructive pulmonary disease (COPD). We observed and compared the evolution of the pathology in two mouse models of COPD induced by cigarette smoke (CS) exposure alone or in combination with lipopolysaccharide (LPS)

Methods

Results

Conclusion