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Background <p>Despite the high prevalence of pediatric asthma, the molecular basis of its pathogenesis remains incompletely understood, in part due to the complex and heterogeneous nature of the disease.</p> Methods <p>In this study, we performed bulk RNA sequencing of peripheral blood mononuclear cells (PBMCs) from 183 children (114 asthma cases, 69 controls) across two independent cohorts as a minimally invasive approach to capture the gene expression changes underlying asthma status and severity.</p> Results <p>Our analysis identified robust signatures of pediatric asthma, including differential expression of a canonical asthma gene (<i>RAB7B</i>) and two novel genes (<i>RPP38-DT</i>, <i>NCAL1</i>), which encode long non-coding RNAs. Additionally, severity-stratified analyses revealed upregulation of several immune-related genes (<i>CCL8</i>, <i>ACOD1</i>, <i>CXCL9</i>, <i>SLAMF1</i>, <i>EPN2</i>) and downregulation of an uncharacterized transcript (<i>ENSG00000288973</i>) as asthma severity increased. Enrichment and co-expression analysis further implicate impaired type I interferon signaling in asthma disease severity.</p> Conclusions <p>Our results demonstrate contributions to the pathobiology of asthma among several novel molecular candidate genes, which may support future efforts towards molecular stratification of pediatric asthma.</p>

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Transcriptomic profiling of pediatric asthma by diseases state and severity

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月20日

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  • Jihoon Kim,
  • Jelte Kelchtermans,
  • Frank Mentch,
  • Fengxiang Wang,
  • James Snyder,
  • Yichuan Liu,
  • Joseph Glessner,
  • Hakon Hakonarson

摘要

Background

Despite the high prevalence of pediatric asthma, the molecular basis of its pathogenesis remains incompletely understood, in part due to the complex and heterogeneous nature of the disease.

Methods

In this study, we performed bulk RNA sequencing of peripheral blood mononuclear cells (PBMCs) from 183 children (114 asthma cases, 69 controls) across two independent cohorts as a minimally invasive approach to capture the gene expression changes underlying asthma status and severity.

Results

Our analysis identified robust signatures of pediatric asthma, including differential expression of a canonical asthma gene (RAB7B) and two novel genes (RPP38-DT, NCAL1), which encode long non-coding RNAs. Additionally, severity-stratified analyses revealed upregulation of several immune-related genes (CCL8, ACOD1, CXCL9, SLAMF1, EPN2) and downregulation of an uncharacterized transcript (ENSG00000288973) as asthma severity increased. Enrichment and co-expression analysis further implicate impaired type I interferon signaling in asthma disease severity.

Conclusions

Our results demonstrate contributions to the pathobiology of asthma among several novel molecular candidate genes, which may support future efforts towards molecular stratification of pediatric asthma.