Journal of thoracic disease · 2025
A new mouse model of biomass smoke-related chronic obstructive pulmonary disease combining porcine pancreatic elastase nebulization.
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Lin Jiaqi, Li Qiumeng, Chen Yating, Lai Jianxiong, Lin Yiqi, Zhao Dongxing
Аннотация
BACKGROUND: Biomass smoke exposure (BME) is an independent risk factor for chronic obstructive pulmonary disease (COPD), particularly among women and children in developing countries. Existing animal models of biomass smoke-related COPD are limited due to prolonged modeling periods. This study aimed to develop a novel composite protocol for constructing a biomass smoke-related COPD mouse model using porcine pancreatic elastase nebulization.
METHODS: Six-week-old female C57BL/6 mice (n=6 per group) were exposed to porcine pancreatic elastase nebulization on the first day and biomass smoke for the remaining 6 days of each week over a 4-month period. Pulmonary function, histopathology, and inflammatory markers were assessed via pulmonary function tests, Hematoxylin & eosin (H&E) staining, enzyme-linked immunosorbent assay (ELISA) and multiplexed liquid chip analysis respectively.
RESULTS: BME induced significant pulmonary function impairment, characterized by increased functional residual capacity (FRC), quasi-static compliance, and static compliance, alongside reduced a ratio of forced expiratory volume at 100 ms and forced vital capacity (FEV100/FVC), dynamic pulmonary compliance as well. Histopathological analysis revealed emphysema and bronchiectasis in lung tissue. Elevated levels of interleukin-1β (IL-1β) and interleukin-10 (IL-10) were observed in the BME group, with a concurrent increase in plasma interleukin-2 (IL-2). In the BME group, mitogen-activated protein kinase 1 (MAPK1) expression increased, whilst expression of signal transducer and activator of transcription 3 (STAT3) decreased. Additionally, matrix metalloproteinase-9 (MMP9) expression decreased.
CONCLUSIONS: The results of this study indicate that BME significantly induced pulmonary function injury leading to emphysema and bronchiectasis changes, as well as systemic inflammation. IL-10 may play a significant role in the pro-inflammatory/anti-inflammatory mechanisms of COPD by regulating the expression of key signalling pathway proteins. A novel COPD modeling method incorporating elastase was constructed.
METHODS: Six-week-old female C57BL/6 mice (n=6 per group) were exposed to porcine pancreatic elastase nebulization on the first day and biomass smoke for the remaining 6 days of each week over a 4-month period. Pulmonary function, histopathology, and inflammatory markers were assessed via pulmonary function tests, Hematoxylin & eosin (H&E) staining, enzyme-linked immunosorbent assay (ELISA) and multiplexed liquid chip analysis respectively.
RESULTS: BME induced significant pulmonary function impairment, characterized by increased functional residual capacity (FRC), quasi-static compliance, and static compliance, alongside reduced a ratio of forced expiratory volume at 100 ms and forced vital capacity (FEV100/FVC), dynamic pulmonary compliance as well. Histopathological analysis revealed emphysema and bronchiectasis in lung tissue. Elevated levels of interleukin-1β (IL-1β) and interleukin-10 (IL-10) were observed in the BME group, with a concurrent increase in plasma interleukin-2 (IL-2). In the BME group, mitogen-activated protein kinase 1 (MAPK1) expression increased, whilst expression of signal transducer and activator of transcription 3 (STAT3) decreased. Additionally, matrix metalloproteinase-9 (MMP9) expression decreased.
CONCLUSIONS: The results of this study indicate that BME significantly induced pulmonary function injury leading to emphysema and bronchiectasis changes, as well as systemic inflammation. IL-10 may play a significant role in the pro-inflammatory/anti-inflammatory mechanisms of COPD by regulating the expression of key signalling pathway proteins. A novel COPD modeling method incorporating elastase was constructed.