Public knowledge document

A spatial sequencing atlas of age-induced changes in the lung during influenza infection.

Influenza virus infection causes increased morbidity and mortality in the elderly. Aging impairs the immune response to influenza, both intrinsically and because of altered interactions with endothelial and pulmonary epithelial cells. To characterize these changes, we performed single-cell RNA sequencing (scRNA-seq), spatial transcriptomics, and bulk RNA sequencing (bulk RNA-seq) on lung tissue from young and aged female mice at days 0, 3, and 9 post-influenza infection. Our analyses identified dozens of key genes differentially expressed in kinetic, age-dependent, and cell type-specific manners. Aged immune cells exhibited altered inflammatory, memory, and chemotactic profiles. Aged endothelial cells demonstrated characteristics of reduced vascular wound healing and a prothrombotic state. Spatial transcriptomics identified novel profibrotic and antifibrotic markers expressed by epithelial and non-epithelial cells, highlighting the complex networks that promote fibrosis in aged lungs.

A spatial sequencing atlas of age-induced changes in the lung during influenza infection.

> 商业许可源文 · EUROPE_PMC · [CC-BY](https://creativecommons.org/licenses/by/)

书目信息

  • 引用:Kasmani MY, Topchyan P, Brown AK, Brown RJ, Wu X, Chen Y, Khatun A, Alson D, Wu Y, Burns R, Lin CW, Kudek MR, Sun J, Cui W. (2023). A spatial sequencing atlas of age-induced changes in the lung during influenza infection. Nature communications. PMID 37852965 · PMC10584893 · DOI 10.1038/s41467-023-42021-y
  • 证据类型:DATABASE_RESOURCE
  • 主题:rna-seq、single-cell、spatial-omics
  • 被引次数(采集时):37
  • 原始记录:[Europe PMC](https://europepmc.org/article/MED/37852965)
  • 来源许可:[CC-BY](https://creativecommons.org/licenses/by/)
  • 作者摘要(按来源许可复用)

    Influenza virus infection causes increased morbidity and mortality in the elderly. Aging impairs the immune response to influenza, both intrinsically and because of altered interactions with endothelial and pulmonary epithelial cells. To characterize these changes, we performed single-cell RNA sequencing (scRNA-seq), spatial transcriptomics, and bulk RNA sequencing (bulk RNA-seq) on lung tissue from young and aged female mice at days 0, 3, and 9 post-influenza infection. Our analyses identified dozens of key genes differentially expressed in kinetic, age-dependent, and cell type-specific manners. Aged immune cells exhibited altered inflammatory, memory, and chemotactic profiles. Aged endothelial cells demonstrated characteristics of reduced vascular wound healing and a prothrombotic state. Spatial transcriptomics identified novel profibrotic and antifibrotic markers expressed by epithelial and non-epithelial cells, highlighting the complex networks that promote fibrosis in aged lungs. Bulk RNA-seq generated a timeline of global transcriptional activity, showing increased expression of genes involved in inflammation and coagulation in aged lungs. Our work provides an atlas of high-throughput sequencing methodologies that can be used to investigate age-related changes in the response to influenza virus, identify novel cell-cell interactions for further study, and ultimately uncover potential therapeutic targets to improve health outcomes in the elderly following influenza infection.

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    A spatial sequencing atlas of age-induced changes in the lung during influenza infection. · GeniOmics