Myd88-dependent positioning of Ptgs2-expressing stromal cells maintains colonic epithelial proliferation during injury
J. Clin. Invest. Sarah L. Brown, et al. 117:258 doi:10.1172/JCI29159 [Go to this article.]

Figure 1
Myd88^–/– and Ptgs2^–/– mouse rectums were susceptible to DSS-induced injury. (A) Colon whole mount from an adult WT B6 mouse treated with 2.5% DSS for 1 week. The DSS-induced lesions (top) and the corresponding anatomic locations (bottom) are indicated. All strains analyzed in this study showed multiple small (<0.5 mm in diameter) ulcers with heaped borders in the descending colon and a confluent ulcer that extended from the ano-rectal junction proximally (0.5–1.0 cm). The intervening area in the remaining rectum (yellow boxed area) was spared of ulcerative injury. (B–G) H&E-stained sections of the rectums from adult B6 WT (B and C), Myd88^–/– (D and E), and Ptgs2^–/– (F and G) mice. (B, D, and F) Untreated mice. (C, E, and G) Mice treated for 7 days with 2.5% DSS in the drinking water. The rectums from WT DSS-treated mice were indistinguishable from those of untreated WT mice. However, DSS-treated Myd88^–/– and Ptgs2^–/– mice both showed a similar pattern of crypt area loss manifested by alterations in crypt morphology (including angulation and dilation of the base; arrows) as compared with untreated controls. Scale bars: 1 cm (A), 100 μm (B–G).