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. 2019 Nov;189(11):2221–2232. doi: 10.1016/j.ajpath.2019.07.017

Figure 1.

Figure 1

Immune cell–generated reactive oxygen influences disease activity and Crk-associated substrate (Cas) phosphorylation in an injured intestinal mucosa. A: Total body weight as a percentage of starting weight of wild-type (WT) and gp91phox-null mice during the treatment of 3% dextran sulfate sodium (DSS)–induced colitis. B: Disease activity index of mice described in A during the treatment of 3% DSS-induced colitis. A and B: The area under the curve was calculated for each mouse, and a P value comparing the groups was obtained by a two-tailed t-test: P = 0.085 (A) and P = 0.026 (B). A and B: Asterisks (A) and daggers (B) represent time points at which groups were different. C: Survival of mice described in A during the treatment of 3% DSS-induced colitis. The Mantel-Cox log-rank test was used to compare the two curves (P = 0.057). D: Immunofluorescence analysis of phosphorylated Cas (green) and E-cadherin (red) after injury to the intestinal mucosa by biopsy wounding in wild-type C57BL/6, gp91phox−/−-null, and neutrophil-depleted mice. DNA is stained with DAPI (blue). Inset in first panel of D shows an enlarged view of the smaller boxed area, magnifying the image at the epithelial cell layer. Note strong expression of Cas-Y410 at the basolateral end of wild-type epithelial cells adjacent to the biopsy wound. This expression was absent in biopsy wounds inflicted on gp91phox−/−- or neutrophil-depleted mice. n = 8 (AC). *P < 0.05 (analysis of variance); P < 0.05 (two-tailed t-test). Scale bars = 100 μm (D).