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Therapeutic Evaluation of Fecal Microbiota Transplantation in an Interleukin 10-Deficient Mouse Model
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Gene expression patterns in experimental colitis in IL-10-deficient mice.

Jonathan J Hansen1, Lisa Holt, R Balfour Sartor

  • 1Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.

Inflammatory Bowel Diseases
|January 13, 2009
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Summary

This study reveals novel gene expression changes in spontaneous colitis. Highly upregulated genes like aquaporin-4 and mitochondrial ribosomal protein-L33 offer new insights into inflammatory bowel disease.

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Area of Science:

  • Genomics
  • Inflammatory Bowel Disease Research
  • Animal Models of Colitis

Background:

  • Previous studies focused on human inflammatory bowel diseases or chemically induced colitis in animals.
  • A genome-wide gene expression comparison in genetically susceptible animals with spontaneous colitis was lacking.

Purpose of the Study:

  • To perform a genome-wide comparison of gene expression in spontaneous colitis using a genetic mouse model.
  • To identify novel genes and pathways involved in the development of inflammatory bowel disease.

Main Methods:

  • Microarray analysis of cecal specimens from IL10-deficient (IL10-/-) mice with spontaneous colitis and wildtype (WT) mice.
  • Validation of gene expression using real-time polymerase chain reaction (PCR) and immunofluorescence microscopy.
  • Comparison with dextran sodium sulfate (DSS)-induced colitis model and activated epithelial cell lines.

Main Results:

  • IL10-/- mice exhibited greater histological inflammation and IL-12/23p40 secretion compared to WT mice.
  • Mitochondrial ribosomal protein-L33, aquaporin-4, indoleamine-pyrrole-2,3-dioxygenase, and MHC class II were significantly upregulated in IL10-/- mice.
  • MHC II and aquaporin-4 showed specific localization patterns within the colon and cecal epithelial cells, respectively.

Conclusions:

  • Most upregulated genes in experimental colitis are immune-related.
  • Aquaporin-4 and mitochondrial ribosomal protein-L33, previously unassociated with inflammation, were the most highly upregulated genes.
  • These findings suggest novel non-immune targets for therapeutic intervention in inflammatory bowel diseases.