Abstract
The histologic appearance of active ulcerative colitis includes an intense lymphoplasmocytosis limited to the mucosa and submucosa often notable for a neutrophilic infiltrate invading the colonic epithelium (crypt abscess). Multiple investigators have shown that the colonic epithelium is in a hyperproliferative state with expansion of the proliferative compartment from the lower crypt to the upper crypt extending to the surface epithelium (1,2). This hyperproliferative state is independent of the degree of inflammation and the duration of the disease and exists even when the disease is in a quiescent state (1,2). Similar hyperproliferative states have been observed in patients at risk for colonic malignancy such as in familial polyposis coli, sporadic colon adenomas, and familial nonpolyposis colon cancer (3). An intriguing observation made by Scheppach et al. (4) is that the labeling index of colonocytes in the upper crypt of patients with ulcerative colitis fell to that of normal healthy controls after treatment with butyrate enemas. This suggests that butyrate may fundamentally alter the state of proliferation, and perhaps differentiation, of colonic epithelial cells in ulcerative colitis.
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Huang, N., Wu, G.D. (1997). Short Chain Fatty Acids Inhibit the Expression of the Neutrophil Chemoattractant, Interleukin 8, in the Caco-2 Intestinal Cell Line. In: Kritchevsky, D., Bonfield, C. (eds) Dietary Fiber in Health and Disease. Advances in Experimental Medicine and Biology, vol 427. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5967-2_16
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DOI: https://doi.org/10.1007/978-1-4615-5967-2_16
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