| First Author | Mannick EE | Year | 2005 |
| Journal | J Gastroenterol Hepatol | Volume | 20 |
| Issue | 3 | Pages | 371-80 |
| PubMed ID | 15740479 | Mgi Jnum | J:97866 |
| Mgi Id | MGI:3576543 | Doi | 10.1111/j.1440-1746.2005.03573.x |
| Citation | Mannick EE, et al. (2005) Altered phenotype of dextran sulfate sodium colitis in interferon regulatory factor-1 knock-out mice. J Gastroenterol Hepatol 20(3):371-80 |
| abstractText | Abstract Background and Aims: Interferon regulatory factor-1 (IRF-1) is a transcription factor with antiviral, proinflammatory and tumor suppressor properties. We examined the role of IRF-1 in dextran sulfate sodium colitis, a murine model of inflammatory bowel disease, to determine if absence of the gene would protect against colitis. Methods: C57BL/6J mice with a targeted disruption of IRF-1 and wild-type C57BL/6J controls received five 7-day cycles of 2% dextran sulfate sodium alternating with five 7-day cycles of water. Colonic tissue was formalin fixed for histological analysis and total RNA extracted for gene chip and SYBR green real-time polymerase chain reaction (PCR) analysis. Results: Histological analysis revealed increased distortion of crypt architecture in the dextran sulfate sodium-treated, IRF-1 -/- animals as compared to dextran sulfate sodium-treated wild-type animals. Five of 15 dextran sulfate sodium-treated IRF-1 -/- mice, but only one of 14 dextran sulfate sodium-treated wild-type mice, developed colonic dysplasia. Microarray analysis comparing colonic gene expression in IRF-1 -/- and wild-type animals revealed decreased expression of caspases, genes involved in antigen presentation, and tumor suppressor genes in the IRF-1 -/- animals. Increased expression of genes involved in carcinogenesis and immunoglobulin and complement genes was also noted in the knock-out animals. Conclusions: Absence of IRF-1 is not protective in dextran sulfate sodium colitis. |
