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PM2.5 Induces Cell-Specific Transcriptomic Alterations in the Lungs of Juvenile Mice
1Department of Respiratory Medicine, Haihe Hospital, Tianjin University, Tianjin, People's Republic of China.
Introduction:
Fine particulate matter (PM2.5) is a major environmental pollutant associated with significant respiratory morbidity in children. However, its cell-type-specific effects on the lungs and the underlying molecular mechanisms remain poorly defined.
Methods:
This study established a juvenile mouse model of PM2.5 airway exposure to assess transcriptional alterations in lung cells via single-cell RNA sequencing (scRNA-seq). Differentially expressed genes were subjected to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. Lung histopathology was evaluated through hematoxylin and eosin staining.
Results:
Histological staining indicated that PM2.5 inhalation induces structural damage in the lung tissue. ScRNA-seq analysis revealed that macrophages, dendritic cells (DCs), lymphocytes, epithelial cells, and stromal cells in the lungs of juvenile mice exhibited the most prominent differential gene expression following PM2.5 instillation, whereas B cells and endothelial cells showed the least. In particular, GO and KEGG analyses indicated that alveolar macrophages exhibited significant upregulation of oxidative phosphorylation (OXPHOS) pathways and downregulation of antibacterial defense mechanisms. CD209+ DCs showed suppressed antigen presentation and altered energy metabolism, primarily via enhanced OXPHOS. Lymphocytes, including NK and CD4+ T cells, displayed modest dysregulation in ribosomal activity. Among non-immune cells, ciliated cells activated interferon signaling, while adventitial fibroblasts showed increased ribosomal protein translation and calcium ion channel regulation. PM2.5 exposure also reshaped cell-cell communication networks, particularly involving alveolar macrophages and immune cells.
Conclusion:
These findings reveal cell-type-specific transcriptomic responses to PM2.5 in juvenile lungs, emphasizing its potential to disrupt immune homeostasis and contribute to pulmonary disease development in children.
Insights
Fine particulate matter (PM2.5) exposure damages juvenile lungs, altering gene expression in immune and structural cells. This disruption impacts immune responses and energy metabolism, potentially leading to pediatric respiratory diseases.
Area of Science:
- Environmental Health
- Pulmonology
- Toxicology
Background:
- Fine particulate matter (PM2.5) is a significant environmental pollutant linked to childhood respiratory issues.
- The specific cellular impacts and molecular mechanisms of PM2.5 in pediatric lungs are not well understood.
Purpose of the Study:
- To investigate the cell-type-specific transcriptional effects of PM2.5 exposure in juvenile mouse lungs.
- To elucidate the molecular pathways affected by PM2.5 in different lung cell populations.
Main Methods:
- Established a juvenile mouse model for PM2.5 airway exposure.
- Utilized single-cell RNA sequencing (scRNA-seq) to analyze transcriptional changes.
- Performed Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses.
- Evaluated lung histopathology using hematoxylin and eosin staining.
Main Results:
- PM2.5 inhalation caused structural lung damage.
- Macrophages, dendritic cells, lymphocytes, epithelial cells, and stromal cells showed significant gene expression changes.
- Alveolar macrophages exhibited altered oxidative phosphorylation and suppressed antibacterial defenses.
- Dendritic cells displayed impaired antigen presentation and modified energy metabolism.
- Ciliated cells activated interferon signaling, and fibroblasts showed altered protein translation and ion channel regulation.
- PM2.5 exposure altered cell-cell communication networks, especially involving macrophages and immune cells.
Conclusions:
- PM2.5 exposure induces distinct transcriptomic responses in various juvenile lung cell types.
- These alterations disrupt immune homeostasis and may contribute to pediatric pulmonary disease development.
