Figure 2. Endogenous glucocorticoids are required to suppress SPEM and gastric inflammation.

Analysis of the gastric corpus lesser curvature from mice euthanized 2 months after sham surgery or adrenalectomy or from adrenalectomized mice treated with corticosterone (cort) for 2 months. (A–D) Immunostaining of stomach sections probed for (A) ATP4B (parietal cells, red), GSII lectin (mucous neck cells, pink), and MIST1(chief cells, green), (B) the SPEM marker CD44 variant 9 (green) and GSII lectin (pink), (C) KI67 (green) and CTNNB1 (epithelial cells, red), or for CD45 (leukocytes, green). Nuclei are stained with DAPI (blue). Scale bars: 100 μm (inset in C: 25 μm). (E) Quantitation of the number of parietal cells, chief cells, and proliferating epithelial cells observed per ×20 field within the lesser curvature (n ≥ 6 mice/group). (F) Quantitative RT-PCR of the SPEM marker genes: Wfdc2, Olfm4, and Cftr using RNA isolated from the gastric corpus lesser curvature (n = 4 mice/group). Data are mean ± SD; P values were determined by 1-way ANOVA with post hoc Tukey’s t test. *P ≤ 0.01, **P ≤ 0.001, ***P ≤ 0.0001.