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. 2019 Oct 23;217(1):e20182325. doi: 10.1084/jem.20182325

Figure 3.

Figure 3.

Chronic gastritis in GEC C1galt1−/− mice is driven by mucosal inflammasomes. (A) Western blot analysis of stomach lysates. p10 is the activated form of Casp1. (B) Densitometry of the Casp1 p10 subunit visualized via Western blot of stomach lysates over time. (C) Enzyme-linked immunosorbent assay of gastric organ culture supernatants (mean ± SD, n = 5 mice/group). (D) IF staining for Casp1 in gastric antrum sections. Arrow indicates carcinoma. Scale bars, 50 µm. (E) Generation of inflammasome-deficient GEC C1galt1−/− mice. (F) Representative macroscopic and histological images of murine stomach. Arrow, inflamed region. Scale bars, gross morphology, 1 cm; others, 50 µm. a, antrum; c, corpus; d, duodenum; f, forestomach. (G) Histological gastritis score among WT, KO, and TKO mice (means ± SD, n = 4–5 mice/group). (H) IF for myeloperoxidase (MPO) in gastric antrum sections of 6-mo-old mice. Scale bars, 20 µm. (I) Enumeration of MPO+ cells in mucosa (n = 4 mice/group). HPF, high-power field. (J) qPCR analysis of stomach lysates derived from 6-mo-old mice (means ± SD, n = 4–5 mice/group). Data are representative of two independent experiments. *, P < 0.05.