Spatial analysis of young and old murine lungs exposed to ozone and fibrogenic stress [spatial_ozone]
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ABSTRACT:
PROVIDER: PRJNA1139846 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29974500_1.fastq.gz | Fastqsanger.gz | |||
| SRR29974500_2.fastq.gz | Fastqsanger.gz | |||
| SRR29974501_1.fastq.gz | Fastqsanger.gz | |||
| SRR29974501_2.fastq.gz | Fastqsanger.gz | |||
| SRR29974502_1.fastq.gz | Fastqsanger.gz |
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Project description:Ozone (O3) is a ubiquitous pollutant known to produce acute and transient inflammation through oxidative injury and inflammation. These effects are exacerbated in susceptible populations, such as the elderly and those exhibiting genetic mutations in central nodes of pulmonary function. To comprehend the impact of these predisposing factors, the present study examines structural, mechanical, and immunological responses to single acute O3 exposure (0.8 ppm, 3h) in young (12 week old) and old (80 week old) mice. We therefore examined the impact of ozone in a surfactant competent and mutant murine line. The latter models a clinically relevant mutation in the gene encoding for the alveolar epithelial type 2 specific surfactant protein C. Ozone exposure produced focal injury localized at the terminal bronchiole-to-alveolar junctions and enlarged alveoli in aged SP-C mutant lungs. This histological feature was used to select regions of interest for spatial transcriptomics. Paraffin sections of 4 mice were prepared: a young/12wk SP-C wild type air control, a young/12wk SP-C wild type ozone (0.8 ppm, 3h), a young/12wk SP-C mutant ozone, and an old/80wk ozone. Immunofluorescence for DNA, CD45, CD68 was performed to identify macrophages (CD45+CD68+) and non-immune ("other", DNA+CD45-) cells within healthy (air control only), peri-injured and injured regions of the lung. A total of 24 regions (680um x 700um in size) were selected from CD68+ macrophages and CD45- non immune/"other" cells. RNA sequencing was then performed. Principal component and pathway analysis revealed spatial heterogeneity in response to ozone, as well as a senescence signature in the aging lungs. These results illustrate regional and age dependent heterogeneity in immune and non-immune cells of the lung during an acute exposure to air pollution.
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Project description:Ozone is known to cause lung injury and resident cells of the respiratory tract, i.e., epithelial cells and macrophages, respond to inhaled ozone in a variety of ways that affect their survival, morphology, and functioning. However, complete understanding of sex-associated and cell type-specific gene expression changes in response to ozone exposure is still limited. Through transcriptome profiling, we aimed to analyze gene expression alterations and biological pathways enrichment in three distinct cell type-enriched compartments of ozone-exposed murine lungs. We chronically exposed adult males and females to 0.8ppm ozone or filtered air. RNA-Seq was performed on airway epithelium-enriched airways, parenchyma, and purified airspace macrophages. Differential gene expression and biological pathway analyses were performed and supported by cellular and immunohistochemical analyses. While majority of differentially expressed genes (DEGs) in ozone-exposed versus air-exposed groups were common between both sexes, sex-specific DEGs were also identified in all the three tissue compartments. As compared to ozone-exposed males, ozone-exposed females had significant alterations in gene expression in three compartments. Pathways relevant to cell division and DNA repair were enriched in the ozone-exposed airways indicating ozone-induced airway injury and repair which was further supported by immunohistochemical analyses. In addition to cell division and DNA repair pathways, inflammatory pathways were also enriched within the parenchyma supporting contribution by both epithelial and immune cells. Finally, immune response and cytokine-cytokine receptor interactions were enriched in macrophages, indicating ozone-induced macrophage activation. Lastly, our analyses also revealed the overall upregulation of mucoinflammation and mucous cell metaplasia-associated pathways.
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