Vitamin A is essential to mucosal immunity and cell differentiation. The fact that lack of it might involve chronic inflammation\nand increased risk of cancer has been reported. Little is known about the mechanism of vitamin A deficiency in the development\nof colitis and its influence on development of colorectal cancer. To determine the influence of vitamin A deficiency on colitis\nand colorectal cancer development, an experimental study using a colitis mouse model was performed. Dextran sulfate sodium\n(DSS) colitis was induced in vitamin A-deficient and vitamin A-supplemented mice. Further, colorectal carcinoma was induced\nby a combination of azoxymethane preinjection and DSS colitis. Results were compared between the two groups mainly by\nimmunohistochemical analysis. Colitis was more severe and recovery from colitis was slower in vitamin A-deficient mice than in\nvitamin A-supplemented mice. Compared with vitamin A-supplemented mice, vitamin A-deficient mice had decreases in colonic\nsubepithelial myofibroblasts and the ratio of mucosal IgA+/IgG+ cells, increases in CD11c+ dendritic cells, and a higher rate of\ndevelopment of colorectal carcinoma with colitis following azoxymethane. Vitamin A lipid droplets in subepithelial myofibroblasts\nwere decreased in vitamin A-deficient mice, suggesting alterations in colonic crypt niche function.Thus, vitamin A inhibited colitis\nand the development of colorectal cancer.
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