Specifically, there were IL-6 + macrophages and neutrophils ( Figure W2G) and IL-17 + macrophages and lymphocytes ( Figure W2H). In addition to the development of polyps, the remaining non-polypoid colonic epithelium Regorafenib purchase of uPA−/− + DSS mice was given a significantly
higher score for dysplasia compared to WT + DSS mice (P = .0006). Two of 11 WT + DSS mice had occasional foci of mild dysplasia, whereas 10 of 11 uPA−/− + DSS mice showed foci of both mild dysplasia and LGD lesions in their colonic mucosa (excluding polyps; Figure 2A). The histopathologic and immunohistochemical characteristics of non-polypoid epithelial dysplastic lesions were similar to their grade-match counterparts found in the polyps. Thiazovivin ic50 Similarly to WT control mice, uPA−/− controls had no dysplastic lesions in their bowel, indicating that in the absence of inflammatory stimuli,
the deficiency of uPA is not sufficient for colonic neoplasmatogenesis ( Figure 2A). Seven months after the last cycle of DSS treatment, 5 of 11 uPA−/− + DSS mice showed a small-sized solitary residual ulcerative lesion in the last part of the descending colon or in the rectum. This lesion was absent from WT + DSS mice (0 of 11; Figure W3A). Otherwise, the colon of both DSS-treated groups had no signs of remaining colitis. However, the histopathologic score for the presence of resident inflammatory cells in the colonic mucosa and submucosa (excluding polyp, dysplastic, and solitary residual ulcerative colitis areas) was significantly higher in uPA−/− + DSS mice compared to that of
WT + DSS mice (P = .0454; Figure 2A). The uPA−/− and WT untreated control groups had comparable numbers of colonic resident inflammatory Acyl CoA dehydrogenase cells ( Figure 2A). Taken together, these results indicate that 7 months after the DSS-induced episodes of colitis, uPA−/− mice fail to reduce the numbers of colonic inflammatory cells, as close to the untreated control baseline levels, as their WT counterparts. In addition, uPA deficiency alone, in the absence of colitogenic stimuli, does not affect residential colonic inflammatory cells. To quantify more accurately this result, we next performed morphometric counts of immunohistochemically labeled immune cells. We found that uPA−/− + DSS mice had significantly more MPO + neutrophils (P = .0002; Figure 2B), F4/80 + macrophages (P = .0008; Figure 2B), IL-6 + (P = .0015; Figure W3B), and IL-17 + (P = .0009; Figure W3B) cells in the colon and significantly more Foxp3 + Treg in the colon (P = .0046; Figure 2B) and the MLN (P = .0185; Figure W3C) compared to WT + DSS mice. By contrast, the total number of CD3 + T-helper lymphocytes was higher in the colon of WT + DSS mice reaching, however, no statistical significance (P = .0818; Figure W3B). The presence of c-kit + mast cells was unremarkable in both groups.
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