解密二氧化硅颗粒诱导的肺纤维化中纤维化微环境的空间组织。

Journal of hazardous materials Pub Date : 2024-10-05 Epub Date: 2024-08-22 DOI:10.1016/j.jhazmat.2024.135540
Liliang Yang, Xinyan Wei, Piaopiao Sun, Jing Wang, Xinbei Zhou, Xinxin Zhang, Wei Luo, Yun Zhou, Wei Zhang, Shencun Fang, Jie Chao
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引用次数: 0

摘要

矽肺是在生产环境中吸入二氧化硅颗粒而诱发的一种间质性肺病。二氧化硅诱导的肺纤维化的一个主要病理特征是局部组织异质性,由于失去了重要的空间背景,这给转录组数据分析带来了巨大挑战。为了解决这个问题,我们将空间基因表达数据与单细胞分析相结合,详细绘制了纤维化区域内部和周围的细胞类型,揭示了正常和患病状态下细胞群的显著变化。此外,我们还利用配体受体图谱探索了纤维化区域内的细胞相互作用,加深了我们对这些区域细胞动态的了解。我们发现了在纤维化微环境中起抑制作用的成纤维细胞亚群,称为 Inmt 成纤维细胞。通过全面的生物信息学、组织学和细胞培养研究来验证我们的发现,突出了单核细胞衍生的巨噬细胞在将 Inmt 成纤维细胞转变为易纤维化的 Grem1 成纤维细胞中的作用,这可能会破坏肺部的稳态以应对外部挑战。因此,我们的研究提供了详细的空间解卷积,显著促进了对肺纤维化发展过程中至关重要的细胞动力学和环境相互作用的理解。
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Deciphering the spatial organization of fibrotic microenvironment in silica particles-induced pulmonary fibrosis.

Silicosis represents a form of interstitial lung disease induced by the inhalation of silica particles in production environments. A key pathological characteristic of silica-induced pulmonary fibrosis is its localized tissue heterogeneity, which presents significant challenges in analyzing transcriptomic data due to the loss of important spatial context. To address this, we integrate spatial gene expression data with single-cell analyses and achieve a detailed mapping of cell types within and surrounding fibrotic regions, revealing significant shifts in cell populations in normal and diseased states. Additionally, we explore cell interactions within fibrotic zones using ligand-receptor mapping, deepening our understanding of cellular dynamics in these areas. We identify a subset of fibroblasts, termed Inmt fibroblasts, that play a suppressive role in the fibrotic microenvironment. Validating our findings through a comprehensive suite of bioinformatics, histological, and cell culture studies highlights the role of monocyte-derived macrophages in shifting Inmt fibroblast populations into profibrotic Grem1 fibroblast, potentially disrupting lung homeostasis in response to external challenges. Hence, the spatially detailed deconvolution offered by our research markedly advances the comprehension of cell dynamics and environmental interactions pivotal in the development of pulmonary fibrosis.

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