<p>Necrotizing enterocolitis (NEC) is a severe inflammatory disorder of the intestine that affects neonatal babies, with a mortality rate of 30–50%. Despite the severe nature of the disease, its rare incidence and early onset prevent further understanding of its etiology and the development of treatment strategies. To further understand the pathogenic mechanism of this disease, we subjected intestinal tissues from ten NEC patients and three control individuals to RNA-sequencing. Clustering of the affected tissues revealed three clusters, each with a distinct transcriptional profile characterized by the expression of genes enriched in inflammatory pathways related to lipid binding and no obvious expression signature. The three subtypes displayed distinct gene expression patterns specific to the cell types composing the small intestine layers. Our results elucidate the genetic rationale underlying patient-specific symptoms, prognosis.</p>

错误:搜索内容不能为空,请输入英文关键词
错误:关键词超出字数限制,请精简
高级检索

Transcriptional stratification of necrotizing enterocolitis identifies distinct disease subtypes

  • Jean Lee,
  • So Hyun Nam,
  • Dayoung Ko,
  • Joong Kee Youn,
  • Jaemoon Koh,
  • Hee Beom Yang,
  • Murim Choi,
  • Hyun-Young Kim

摘要

Necrotizing enterocolitis (NEC) is a severe inflammatory disorder of the intestine that affects neonatal babies, with a mortality rate of 30–50%. Despite the severe nature of the disease, its rare incidence and early onset prevent further understanding of its etiology and the development of treatment strategies. To further understand the pathogenic mechanism of this disease, we subjected intestinal tissues from ten NEC patients and three control individuals to RNA-sequencing. Clustering of the affected tissues revealed three clusters, each with a distinct transcriptional profile characterized by the expression of genes enriched in inflammatory pathways related to lipid binding and no obvious expression signature. The three subtypes displayed distinct gene expression patterns specific to the cell types composing the small intestine layers. Our results elucidate the genetic rationale underlying patient-specific symptoms, prognosis.