biostudies-literatureHansen JJNCRR NIH HHSNIDDK NIH HHS890-9https://www.ebi.ac.uk/biostudies/studies/S-EPMC2763592biostudies-literatureUnknown15(6)<h4>Background</h4>While others have described gene expression patterns in humans with inflammatory bowel diseases and animals with chemically induced colitis, a genome-wide comparison of gene expression in genetically susceptible animals that develop spontaneous colitis has not been reported.<h4>Methods</h4>We used microarray technology to compare gene expression profiles in cecal specimens from specific pathogen-free IL10-deficient (IL10-/-) mice with colitis and normal wildtype (WT) mice. RNA isolated from ceca of IL10-/- and WT mice was subjected to microarray analysis. The results were confirmed by real-time polymerase chain reaction (PCR) and immunofluorescence microscopy of selected molecules. Expression of the selected genes in dextran sodium sulfate (DSS)-treated mice with colitis and epithelial cell lines activated with pathophysiologic stimuli was measured by real-time PCR.<h4>Results</h4>Histological inflammation of the colon and IL-12/23p40 secretion from intestinal explants were greater in IL10-/- and DSS-treated mice versus WT and untreated mice. Microarray analysis demonstrated >10-fold induction of the following molecules in the ceca of IL10-/- mice: mitochondrial ribosomal protein-L33, aquaporin-4, indoleamine-pyrrole-2,3-dioxygenase, and MHC class II with 63, 25, 20, and 12-fold increases, respectively. Cytochrome-P450, pancreatic lipase-related protein-2, and transthyretin were downregulated in IL10-/- mice. MHC II was increased throughout the colon, and aquaporin-4 was increased in the basolateral aspect of cecal epithelial cells. MHC II mRNA was increased in epithelial cells treated with IFN-gamma, but not TNF or Toll-like receptor ligands.<h4>Conclusions</h4>Although most upregulated genes in experimental colitis are immune-related, aquaporin-4 and mitochondrial ribosomal protein-L33, which have not been previously associated with inflammation, were most highly upregulated.Inflammatory bowel diseasesGene expression patterns in experimental colitis in IL-10-deficient mice.PMC2763592T32 DK007737P30 DK34987P40 RR018603-05P30 DK034987P20 RR 020764-02P20 RR020764P40 RR018603P40 RR 018603R01 DK53347R01 DK053347Holt LHansen JJSartor RBfalseGene expression patterns in experimental colitis in IL-10-deficient mice.<h4>Background</h4>While others have described gene expression patterns in humans with inflammatory bowel diseases and animals with chemically induced colitis, a genome-wide comparison of gene expression in genetically susceptible animals that develop spontaneous colitis has not been reported.<h4>Methods</h4>We used microarray technology to compare gene expression profiles in cecal specimens from specific pathogen-free IL10-deficient (IL10-/-) mice with colitis and normal wildtype (WT) mice. RNA isolated from ceca of IL10-/- and WT mice was subjected to microarray analysis. The results were confirmed by real-time polymerase chain reaction (PCR) and immunofluorescence microscopy of selected molecules. Expression of the selected genes in dextran sodium sulfate (DSS)-treated mice with colitis and epithelial cell lines activated with pathophysiologic stimuli was measured by real-time PCR.<h4>Results</h4>Histological inflammation of the colon and IL-12/23p40 secretion from intestinal explants were greater in IL10-/- and DSS-treated mice versus WT and untreated mice. Microarray analysis demonstrated >10-fold induction of the following molecules in the ceca of IL10-/- mice: mitochondrial ribosomal protein-L33, aquaporin-4, indoleamine-pyrrole-2,3-dioxygenase, and MHC class II with 63, 25, 20, and 12-fold increases, respectively. Cytochrome-P450, pancreatic lipase-related protein-2, and transthyretin were downregulated in IL10-/- mice. MHC II was increased throughout the colon, and aquaporin-4 was increased in the basolateral aspect of cecal epithelial cells. MHC II mRNA was increased in epithelial cells treated with IFN-gamma, but not TNF or Toll-like receptor ligands.<h4>Conclusions</h4>Although most upregulated genes in experimental colitis are immune-related, aquaporin-4 and mitochondrial ribosomal protein-L33, which have not been previously associated with inflammation, were most highly upregulated.2009-01-01T00:00:00Z2009 Jun2024-12-04T09:56:36.989Z2019-03-27T00:25:58ZS-EPMC27635921913368910.1002/ibd.20850