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首页> 外文期刊>American Journal of Physiology >Compartment-specific transcriptomics of ozone-exposed murine lungs reveals sex- and cell type-associated perturbations relevant to mucoinflammatory lung diseases
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Compartment-specific transcriptomics of ozone-exposed murine lungs reveals sex- and cell type-associated perturbations relevant to mucoinflammatory lung diseases

机译：臭氧曝光鼠肺的舱特异性转录组织揭示了与粘螨炎症肺病相关的性和细胞类型相关的扰动

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摘要

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, a complete understanding of the sex-associated and the cell type-specific gene expression changes in response to ozone exposure is still limited. Through transcrip-tome profiling, we aimed to analyze gene expression alterations and associated enrichment of biological pathways in three distinct cell type-enriched compartments of ozone-exposed murine lungs. We subchronically exposed adult male and female mice to 0.8 ppm 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 immunohisto-chemical analyses. While a 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 of the three tissue compartments. As compared with 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. Further, immune response and cytokine-cytokine receptor interactions were enriched in macrophages, indicating ozone-induced macrophage activation. Finally, our analyses also revealed the overall upregulation of mucoinflammation- and mucous cell metaplasia-associated pathways following ozone exposure.
机译：众所周知，臭氧会导致肺损伤，呼吸道的常驻细胞（即上皮细胞和巨噬细胞）对吸入臭氧的反应方式多种多样，影响它们的存活、形态和功能。然而，对臭氧暴露引起的性别相关和细胞类型特异性基因表达变化的完整理解仍然有限。通过transcrip-tome分析，我们旨在分析暴露于臭氧的小鼠肺中三种不同细胞类型富集区的基因表达改变和相关的生物途径富集。我们将成年雄性和雌性小鼠亚慢性暴露于0.8 ppm臭氧或过滤空气中。RNA-Seq在气道上皮富集的气道、实质和纯化的巨噬细胞上进行。进行差异基因表达和生物途径分析，并通过细胞和免疫组织化学分析予以支持。虽然在臭氧暴露组和空气暴露组中，大多数差异表达基因（DEG）在两性之间都是常见的，但在所有三个组织室中也发现了性别特异性DEG。与暴露于臭氧的雄性相比，暴露于臭氧的雌性在三个区域的基因表达有显著改变。与细胞分裂和DNA修复相关的途径在暴露于臭氧的气道中富集，表明臭氧诱导的气道损伤和修复，免疫组化分析进一步支持了这一点。除了细胞分裂和DNA修复途径外，炎症途径也在实质内富集，支持上皮细胞和免疫细胞的贡献。此外，免疫反应和细胞因子-细胞因子受体相互作用在巨噬细胞中富集，表明臭氧诱导的巨噬细胞活化。最后，我们的分析还揭示了臭氧暴露后粘液炎症和粘液细胞化生相关途径的整体上调。

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