Fig. 3

PCDH20 deficiency impaired intestinal barrier integrity in colitis. a–e Pcdh20 CKO mice developed more severe colitis than WT mice after DSS administration. Weight loss (a), disease activity index (b), colon length (c), ulcer and pathological score (d), and myeloperoxidase (MPO) activity (e). f Increased FD4 level detected in the serum of Pcdh20 CKO mice with DSS-induced colitis. g,h Pcdh20 CKO mice developed more severe colitis than WT mice after TNBS administration. Shortened colon length, perforation (red arrow), stenosis (blue arrow) (g), greater ulcers, and edema (h). i,j Greater paracellular permeability in PCDH20-deficient Caco-2 cells treated with TNFα (2.5 ng/mL) and IFN-γ (10 ng/mL) compared with control. Transepithelial electrical resistance (TEER) (i), paracellular permeability assessment with FD4(j). k,l Paracellular permeability in PCDH20-dificient Caco-2 cells rescued by transfecting PCDH20 plasmid. TEER (k), paracellular permeability assessment with FD4 (l). Magnification (d–h) × 100, scale bars = 100 μm. The data in a-f, i-l were presented as mean ± SEM. * p < 0.05, **p < 0.01, ***p < 0.001 vs Control. Numbers in each group: a,b dH2O-WT n = 10, dH2O-CKO n = 12, DSS-WT n = 22, DSS-CKO n = 26; c dH2O-CKO n = 12, DSS-CKO n = 11, other groups n = 10; d dH2O-WT n = 3, dH2O-CKO n = 3, DSS-WT n = 10, DSS-CKO n = 12; e dH2O-WT n = 5, dH2O-CKO n = 8, DSS-WT n = 10, DSS-CKO n = 12; f dH2O-WT n = 3, other groups n = 5; g,h Each group n = 3. Intestinal epithelial conditional knockout, CKO; wild-type, WT; overexpression, OE