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Updated: Jul 15, 2025
Lung Fixation under Constant Pressure for Evaluation of Emphysema in Mice
Published on: September 26, 2019
Temporal analysis of lung injury induced by real-ambient PM2 .5 exposure in mice
Huixian Zeng1,2, Wei Chen1,2, Meizhen Li2
1State Key Laboratory of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Abstract:
Fine particulate matter (PM2.5 ) has been shown to induce lung injury. However, the pathophysiological mechanisms of PM2.5 -induced pulmonary injury after different exposure times are poorly understood. In this study, we exposed male ICR mice to a whole-body PM2.5 inhalation system at daily mean concentration range from 92.00 to 862.00 μg/m3 for 30, 60, and 90 days. We found that following prolonged exposure to PM2.5 , pulmonary injury was increasingly evident with significant histopathological alterations. Notably, the pulmonary inflammatory response and fibrosis caused by PM2.5 after different exposure times were closely associated with histopathological changes. In addition, PM2.5 exposure caused oxidative stress, DNA damage and impairment of DNA repair in a time-dependent manner in the lung. Importantly, exposure to PM2.5 eventually caused apoptosis in the lung through upregulation of cleaved-caspase-3 and downregulation of Bcl-2. Overall, our data demonstrated that PM2.5 led to pulmonary injury in a time-dependent manner via upregulation of proinflammatory and fibrosis-related genes, and activation of the DNA damage response. Our findings provided a novel perspective on the pathophysiology of respiratory diseases caused by airborne pollution.
Insights
Fine particulate matter (PM2.5) causes lung injury, inflammation, and fibrosis. This study shows PM2.5 exposure over time leads to DNA damage, oxidative stress, and apoptosis in mouse lungs.
Area of Science:
- Environmental Health
- Toxicology
- Pulmonary Medicine
Background:
- Fine particulate matter (PM2.5) is a known lung injury inducer.
- Mechanisms of PM2.5-induced pulmonary injury over time remain unclear.
Purpose of the Study:
- To investigate the time-dependent pathophysiological mechanisms of PM2.5-induced pulmonary injury.
- To elucidate the role of inflammation, fibrosis, oxidative stress, and DNA damage in PM2.5 toxicity.
Main Methods:
- Male ICR mice were exposed to PM2.5 (92.00–862.00 μg/m³) for 30, 60, and 90 days.
- Histopathological alterations, inflammatory response, fibrosis, oxidative stress, DNA damage, and apoptosis were assessed.
Main Results:
- Prolonged PM2.5 exposure caused progressive histopathological lung injury.
- Increased pulmonary inflammation, fibrosis, oxidative stress, and DNA damage were observed in a time-dependent manner.
- PM2.5 exposure led to lung cell apoptosis via caspase-3 and Bcl-2 pathways.
Conclusions:
- PM2.5 induces pulmonary injury in a time-dependent manner.
- Upregulation of proinflammatory and fibrosis-related genes, and DNA damage response activation are key mechanisms.
- Findings offer insights into respiratory diseases caused by air pollution.
