Fig. 2.

DSS treatment induced symptomatic parameters of colitis-like disease in both genotypes compared to controls. (A, B) DAI was monitored on day 0, during the second cycle of 2%DSS (3 days), and 2 days post DSS exposure in both DSS and vehicle treated groups per genotype, (*p<0.05, ^**p<0.01, ^***p<0.001, ^****p<0.0001 vehicle treated groups vs. DSS treated groups per genotype comparing on the same day, two-way ANOVA multiple comparisons followed by uncorrected Fisher’s LSD test indicate WT DAI F (5, 96) = 15.17 and p (interaction) <0.0001; App^NL-G-F DAI F (5, 108) = 5.272 and p (interaction)= 0.0002, mean ± SEM, n=9–10 animals). (C, D) the percentage of body weight (%BW) changes was calculated during the second DSS exposure untill the week of tissue collection per each treatment groups per genotype, (*p<0.05, ^**p<0.01, ^***p<0.001, ^****p<0.0001 vehicle treated groups vs. DSS treated groups per genotype comparing on the same day, Two-way ANOVA multiple comparisons followed by uncorrected Fisher’s LSD test indicate WT %BW F (9, 160) = 6.897 and p (interaction) <0.0001; App^NL-G-F %BW F (9, 180) = 4.798 and p (interaction) <0.0001, mean ± SEM, n=9–10 animals). (E-G) Spleen and colon weights as well as colon length were measured from WT and App^NL-G-F mice to indicate colonic inflammation, (*p<0.05, ^**p<0.01, ^***p<0.001, Unpaired two-tailed t-test indicate WT spleen weight t(14)=3.007 and p=0.0094; App^NL-G-F spleen weight t(16)=2.741 and p=0.0145; WT colon weight t(12)=5.591 and p=0.0001; App^NL-G-F colon weight t(18)=2.215 and p=0.0399; WT colon length t(16)=4.589 and p=0.0003; App^NL-G-F colon length t(18)=1.614 and p=0.1239, mean ± SEM, n=7–10 animals).