Figure 5.

Conditional deletion of epithelial Vhlh protects from experimental colitis. (A) Vhlh mutant animals (filled circles, n = 12) recovered their initial weight loss after administration of TNBS significantly faster than WT littermates (filled squares, n = 22; P < 0.01 by ANOVA). Values for vehicle control–treated Vhlh mutant and WT animals were combined (open squares). (B) Colonic length was significantly decreased in WT TNBS-treated animals compared with conditional Vhlh mutant animals with TNBS colitis ( P – 0.05 vs. TNBS-treated WT animals, *P – 0.05 vs. vehicle-treated controls). (C) Real-time PCR analysis for GLUT-1, ITF, MDR1, and CD73. Data are presented as fold ± SEM increase over vehicle control–treated WT animals (represented by the line at 1-fold increase). While TNBS treatment significantly induced all 4 genes (*P – 0.05 vs. vehicle-treated WT), such differences were enhanced in conditional Vhlh mutant animals exposed to TNBS in regard to ITF, MDR1, and CD73 ( P – 0.05 vs. TNBS-treated WT, ^–P – 0.05 vs. vehicle-treated Vhlh mutants). (D) Significantly lower flux of the FITC-dextran as a measure of intestinal permeability in TNBS-treated Vhlh mutant compared with TNBS-treated WT animals ( P – 0.05; P not significant for TNBS-treated Vhlh mutants vs. vehicle control–treated mice). As no difference was seen between mutant and WT vehicle control–treated animals (compare with Figure 4E), values were combined.