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Detection of interferon regulatory factor-1 in lamina propria mononuclear cells in Crohn's disease
M Clavell1, H Correa-Gracian, Z Liu
1Louisiana State University Department of Pediatrics, Stanley Scott Cancer Center, New Orleans, USA.
Background:
The transcription factor, interferon regulatory factor (IRF)-1, is stimulated by interferon-gamma and regulates the expression of several genes implicated in the pathogenesis of inflammatory bowel disease, including interleukin-6, major histocompatibility complex class II molecules, and inducible nitric oxide synthase. Interferon regulatory factor-1 also stimulates naive CD4+ T-cells to differentiate into T-helper-1 cells, the T-cell subset that appears to be upregulated in Crohn's disease. The purpose of this study was to examine the expression of IRF-1 in the nuclei of lamina propria mononuclear cells in situ in colonoscopic biopsy specimens from pediatric patients with Crohn's disease, in patients with ulcerative colitis, and in control patients with no histopathologic abnormalities.
Methods:
Archival paraffin-embedded tissue sections were obtained from 25 pediatric patients with Crohn's disease, 6 patients with ulcerative colitis, and 12 control patients who had undergone colonoscopy. Tissue sections were stained with polyclonal rabbit anti-human antisera to IRF-1 and horseradish-peroxidase-conjugated, biotinylated, goat anti-rabbit secondary antibody. Slides were scored and scores compared among patient groups using analysis of variance.
Results:
Patients with Crohn's disease had significantly higher IRF-1 scores (95% confidence interval [CI], 1.70-2.04) than patients with ulcerative colitis (95% CI, 0.92-1.23) or control subjects (95% CI, 1.11-1.52).
Conclusions:
Increased expression of IRF-1 in lamina propria mononuclear cells from patients with Crohn's disease may be relevant to the pathogenesis of Crohn's disease.