Fig. 7: Effect of DCLK1 deletion on mucosal inflammation and colitis.
From: DCLK1 isoforms and aberrant Notch signaling in the regulation of human and murine colitis
Control (floxed) or intestinal epithelial cell-specific DCLK1-KO (DCLK1ΔIEC) or DCLK1Δ IEC;Rag-1−/− double KO (DKO) mice were infected with CR and given single doses of DBZ. Ai, Bi Gross thickening and ulceration of the colon in the two transgenic lines. Aii, Bii Representative histology (H&E) or immunostaining in the paraffin-embedded sections prepared from the distal colons of the indicated mouse groups. Alcian blue and Ki-67 labeling represents goblet and proliferating cells, respectively. Anti-CR- and α-Muc2-stained Citrobacter rodentium and Muc-2, respectively (n = 6 mice/group; Scale bar: 100 μm). C, D Immune cells were FACS-sorted with antibodies against CD11c, F4/80, and Ly6G from the crypt-denuded lamina propria of the indicated groups of mice and the expression of the two isoforms of DCLK1 were measured by RT-qPCR. The values were normalized to GAPDH, and data are presented as fold change. P values for C based on significance: 0.000033 (CD11c: DCLK1-S), 0.000057 (F4/80: DCLK1-S), 0.013 (Ly6G: DCLK1-L), 0.0081 (Ly6G: DCLK1-S). P values for D based on significance: 0.000035 (CD11c: DCLK1-S), 0.016 (F4/80: DCLK1-S), <0.000001 (Ly6G: DCLK1-S); n = 3 independent experiments.
