Figure 4. Atg16L1 mutant mice display a virus-dependent aberrant response to DSS in the colon.
(A) WT and Atg16L1HM mice were orally inoculated with MNV CR6 for 7 days or uninfected, and subsequently given 2.5% DSS for an additional 7 days at which point intestines where harvested. Light microscopy images of H+E stained sections of ulcerated regions located immediately adjacent to the ano-rectal junction are shown. Yellow double-headed arrows indicate the muscularis propria thickness. In the MNV CR6-infected Atg16L1HM sample, lymphoid aggregates are indicated by yellow dashed circles, and the black dashed region contains submusocal fibrosis and inflammation. Scale bar represents 500 μm.
(B) Table summarizing the outcome of DSS treatment. All intestines were harvested at the end of DSS treatment for analysis. + and − refer to the presence or absence of inflammatory hallmarks of Crohn’s disease respectively (n ≥ 6 mice/condition).
(C) Quantification of the muscularis propria thickness in the region adjacent to the anorectal junction from DSS treated mice. 7 days and 0 days refer to the amount of time mice were inoculated with the virus prior to DSS treatment. The Increase in muscle thickness was normalized to the average of uninfected WT mice treated with DSS (*p < 0.05, ***p < 0.001, mean +/−SEM).
(D) Number of lymphoid aggregates in the region adjacent to the ano-rectal junction from DSS treated mice (***p < 0.001, mean +/−SEM). N.D. refers to not detected.
See also Figure S5.