Glucocorticoids restore mucin biosynthesis in intestinal goblet cells with a mucin folding defect. WT C57BL/6 (WT) and Winnie (Win) mice at 4 wk of age were treated with DEX (20 ng/g body weight i.p. daily for 28 d) or vehicle (control) and intestinal tissue sampled (n = 7–8/group, single experiment). (A) Representative AB/PAS stained proximal, mid and distal colon tissue sections from control and DEX-treated WT and Winnie mice. The volume of stored O-glycosylated mucin in each intestinal region as a percentage of total crypt volume is shown at the right. Box plots with whiskers show median, quartiles and the maximum range. Kruskal-Wallis nonparametric analysis, Dunn’s multiple comparison ^#, WT versus Win *, Win versus DEX-treated Win; *, P < 0.05; ^###,***, P < 0.001. (B) Cellular localization of Muc2 in representative mid colon tissue sections of control and DEX-treated WT and Winnie mice was determined by immunohistochemistry with the mM2.2 antibody reactive with the precursor and mature forms of Muc2. (C) Accumulation of Muc2 precursor in representative mid colon tissue sections in control and DEX-treated WT and Winnie mice was assessed by immunohistochemistry with an antibody reactive with the precursor but not the mature form of Muc2. (D) Abundance of the Agr2 protein disulfide isomerize involved in Muc2 biosynthesis in representative mid colon tissue sections in control and DEX-treated WT and Winnie mice was assessed by immunohistochemistry. Bars, 50 µm.