OBJECTIVES AND DESIGN: The present study aimed at a broad genome expression analysis of rat skin and draining lymph nodes affected with allergic contact dermatitis (ACD). METHODS: ACD was elicited in sensitized SD rats with 0.5% 2,4-dinitrofluorobenzene on skin areas distant from the sensitization sites. Involved skin and lymph nodes were dissected 8 and 24 h after challenge. RNA was hybridized on Affymetrix GeneChips. Expression data were analyzed with the GeneSpring software. RESULTS: Expression of 1,882 out of 8,799 examined genes in skin or lymph nodes was significantly (p < or = 0.01) changed compared to levels in normal tissue. After an additional 2- fold filtering, four expression patterns were selected and interpreted. Prominently up-regulated genes were IL-6, CCR-5, CCL-2, CCL-3, CXCL-1, CXCL-10, TIMP-1, OX-40, calgranulin b, ST2, beta-defensin, iNOS, STAT-1, MMP-3, MMP-9, MMP-12, and MMP-13. CONCLUSIONS: In addition to previously reported transcript changes, the present findings suggest/support that plasma cells, mast cells, and a specific IFN-gamma pathway play a substantial role in the pathogenesis of ACD.
OBJECTIVES AND DESIGN: The present study aimed at a broad genome expression analysis of rat skin and draining lymph nodes affected with allergic contact dermatitis (ACD). METHODS: ACD was elicited in sensitized SD rats with 0.5% 2,4-dinitrofluorobenzene on skin areas distant from the sensitization sites. Involved skin and lymph nodes were dissected 8 and 24 h after challenge. RNA was hybridized on Affymetrix GeneChips. Expression data were analyzed with the GeneSpring software. RESULTS: Expression of 1,882 out of 8,799 examined genes in skin or lymph nodes was significantly (p < or = 0.01) changed compared to levels in normal tissue. After an additional 2- fold filtering, four expression patterns were selected and interpreted. Prominently up-regulated genes were IL-6, CCR-5, CCL-2, CCL-3, CXCL-1, CXCL-10, TIMP-1, OX-40, calgranulin b, ST2, beta-defensin, iNOS, STAT-1, MMP-3, MMP-9, MMP-12, and MMP-13. CONCLUSIONS: In addition to previously reported transcript changes, the present findings suggest/support that plasma cells, mast cells, and a specific IFN-gamma pathway play a substantial role in the pathogenesis of ACD.