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Induced Differentiation of M Cell-like Cells in Human Stem Cell-derived Ileal Enteroid Monolayers
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NOD2 status and human ileal gene expression.

Christina M Hamm1, Melissa A Reimers, Casey K McCullough

  • 1Division of Gastroenterology, Washington University, St Louis School of Medicine, St Louis, Missouri, USA.

Inflammatory Bowel Diseases
|February 16, 2010
PubMed
Summary

NOD2 risk alleles are linked to ileal Crohn's disease (CD) inflammation. Gene expression changes in the ileum occur in CD patients, even without NOD2 risk alleles, suggesting broader disease mechanisms.

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Area of Science:

  • Gastroenterology
  • Genetics
  • Molecular Biology

Background:

  • NOD2 single nucleotide polymorphisms (SNPs) are associated with increased risk of ileal Crohn's disease (CD).
  • Understanding the genetic contribution to CD pathogenesis is crucial for developing targeted therapies.

Purpose of the Study:

  • To compare ileal mucosal gene expression in CD patients with and without NOD2 risk alleles.
  • To investigate the role of NOD2 variants in ileal inflammation and gene expression patterns in CD.

Main Methods:

  • Ileal samples were collected from 18 CD patients and 9 controls.
  • Samples were genotyped for major NOD2 risk alleles.
  • Microarray analysis and quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) were used to assess gene expression.

Main Results:

  • 18 genes, including those related to lymphocyte activation, were upregulated in NOD2 risk allele-positive (NOD2(R)) CD patients compared to NOD2 risk allele-negative (NOD2(NR)) CD patients.
  • Altered ileal gene expression was observed in unaffected ileal mucosa of NOD2(NR) CD patients compared to controls.
  • Increased CD3D expression correlated with NOD2(R) status; increased MUC1, DUOX2, DMBT1 and decreased C4orf7 expression were associated with CD independent of NOD2 status.

Conclusions:

  • NOD2 risk alleles contribute to impaired ileal inflammation regulation in CD.
  • Ileal gene expression alterations occur in CD patients independently of NOD2 status, indicating additional disease pathways.