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Genome-wide expression profiles of necrotizing enterocolitis versus spontaneous intestinal perforation in human

Kathy Yuen Yee Chan1, Kam Tong Leung, Yuk Him Tam

  • 1Departments of *Paediatrics †Surgery ‡Anatomical and Cellular Pathology, Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, NT, Hong Kong.

Annals of Surgery
|December 26, 2013
PubMed
Abstract

Insights

Necrotizing enterocolitis (NEC) and spontaneous intestinal perforation (SIP) in preterm infants involve distinct molecular pathways. NEC shows extensive gene changes linked to inflammation and microbial factors, while SIP has milder changes related to muscle contraction and matrix remodeling.

Area of Science:

  • Molecular biology
  • Genomics
  • Neonatal research

Background:

  • Necrotizing enterocolitis (NEC) and spontaneous intestinal perforation (SIP) are critical surgical emergencies in preterm infants.
  • High morbidity and mortality rates are associated with NEC and SIP.
  • The underlying pathophysiology and molecular mechanisms of NEC and SIP remain largely unknown.

Purpose of the Study:

  • To create a comprehensive database of gene regulation in NEC and SIP.
  • To compare differentially regulated molecular networks in human NEC and SIP tissues.
  • To identify distinct molecular signatures for NEC and SIP.

Main Methods:

  • Whole genome microarray analysis of intestinal tissues from NEC, SIP, and control infants.
  • Quantitative polymerase chain reaction (qPCR) for validation of 52 target genes.
  • Construction of regulatory networks based on functional pathways of affected genes.

Main Results:

  • NEC tissues exhibited significant gene expression changes across pathways including angiogenesis, inflammation, hypoxia, and microbial sensing (TLR2, TLR4).
  • Dysregulated genes in NEC were linked to NF-κB, AP-1, and HIF1A transcription factors, indicating microbial and inflammatory involvement.
  • SIP tissues showed less pronounced changes, primarily associated with G-protein signaling, muscle contraction, and extracellular matrix remodeling.

Conclusions:

  • NEC and SIP represent distinct diseases with different etiologies and pathophysiologies.
  • This study provides the first comprehensive database of differential gene expression in human NEC and SIP.
  • Findings may facilitate the development of disease-specific biomarkers and targeted therapies for NEC and SIP.

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