Fig. 7
Contribution of glycosylated LspA-SIGNR1 interaction to protection against DSS-induced colitis. Signr1+/+ and Signr1−/− mice were gavaged with P. UF1, ΔlspA P. UF1 or PBS on days −7, −4, and −1, and 3% DSS was given in drinking water on day 0. Mice continued to receive the bacteria every three days for an additional three times and monitored for disease progression until day 12 (Signr1+/+ mice) or day 10 (Signr1−/− mice due to disease severity). a Weight loss, diarrhea, and fecal blood scores were monitored over time. b Bar graphs showing area under curve (AUC) for diarrhea and FOB scores. c Colon lengths were measured and compared. d Colonoscopies were performed in the indicated groups of mice. e–f Colitis scores based on histopathology of the colons were also used as measures of disease severity. g Serum FITC-dextran levels of DSS-treated Signr1+/+ and Signr1−/− mice gavaged with P. UF1, ΔlspA P. UF1 or PBS. h–i Transcript levels of tight junction proteins in colonic tissues of the indicated groups of mice. Data are pooled from 2 independent experiments (n = 7–8 mice/group). Error bars indicate SEM. **P < 0.01, ***P < 0.001, ****P < 0.0001, ANOVA plus Tukey’s post-test
