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Short-term PM2.5 exposure induces transient lung injury and repair
Yu Li1, Bencheng Lin2, De Hao3
1Department of Basic Medicine, Haihe Hospital, Tianjin University, Tianjin, China; Tianjin Key Laboratory of Lung Regenerative Medicine, Tianjin, China.
Abstract:
Exposure to fine atmospheric particulate matter (PM) is known to induce lung inflammation and injury; however, the way in which sophisticated endogenous lung repair and regenerative programs respond to this exposure remains unknown. In this study, we established a whole-body mouse exposure model to mimic real scenarios. Exposure to fine PM (PM with an aerodynamic diameter ≤ 2.5 µm [PM2.5]; mean 1.05 mg/m3) for 1-month elicited inflammatory infiltration and epithelial alterations in the lung, which were resolved 6 months after cessation of exposure. Immune cells that responded to PM2.5 exposure mainly included macrophages and neutrophils. During PM2.5 exposure, alveolar epithelial type 2 cells initiated rapid repair of alveolar epithelial mucosa through proliferation. However, the reparative capacity of airway progenitor cells (club cells) was impaired, which may have been related to the oxidative production of neutrophils or macrophages, as suggested in organoid co-cultures. These data suggested that the pulmonary toxic effects of short-term exposure to fine atmospheric PM at a certain dosage could be overcome through tissue reparative mechanisms.
Insights
Short-term exposure to fine particulate matter (PM2.5) causes lung inflammation but the lungs can repair themselves. However, airway progenitor cells
Area of Science:
- Environmental Health
- Pulmonary Medicine
- Toxicology
Background:
- Fine atmospheric particulate matter (PM2.5) exposure is a known cause of lung inflammation and injury.
- The endogenous lung repair mechanisms responding to PM2.5 are not fully understood.
Purpose of the Study:
- To investigate the lung's endogenous repair and regenerative response to fine particulate matter (PM2.5) exposure using a whole-body mouse model.
Main Methods:
- Whole-body mouse exposure model to fine PM2.5.
- Analysis of inflammatory infiltration and epithelial alterations post-exposure.
- Assessment of immune cell responses (macrophages, neutrophils).
- Evaluation of alveolar epithelial type 2 cell and club cell proliferation and repair capacity.
- Organoid co-culture experiments to assess oxidative stress impact.
Main Results:
- One-month PM2.5 exposure caused lung inflammation and epithelial changes, which resolved 6 months after exposure cessation.
- Macrophages and neutrophils were the primary immune cells responding to PM2.5.
- Alveolar epithelial type 2 cells showed rapid proliferation for repair, but club cell repair capacity was impaired, potentially due to oxidative stress from immune cells.
- Pulmonary toxic effects from short-term PM2.5 exposure were overcome by tissue repair mechanisms.
Conclusions:
- The lung possesses inherent repair mechanisms capable of resolving inflammation and injury induced by short-term PM2.5 exposure.
- While alveolar epithelial repair is robust, airway progenitor cell (club cell) function may be compromised by PM2.5-induced oxidative stress.
- Understanding these repair dynamics is crucial for mitigating the health impacts of air pollution.
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