Enterochromaffin (EC) cells regulate gut motility and secretion in response to luminal stimuli, via the release of serotonin (5-HT). Inflammatory bowel disease and other gastrointestinal disorders are associated with increased numbers of EC cells and 5-HT availability. Our aim was to determine whether proliferation of EC cells contributed to the hyperplasia associated with intestinal inflammation. Ileitis was induced in guinea-pigs by intraluminal injection of 2,4,6-trinitrobenzene sulphonic acid (TNBS). A single pulse of 5-bromo-2'-deoxyuridine (BrdU) was injected 1 or 24 h before the collection of tissue, 6 or 7 days after TNBS treatment. In the controls, the labelling index (percentage of BrdU-labelled EC cells) was less than 1%. Despite a significant increase in EC cells in the inflamed ileum, the labelling index was similar in the TNBS-treated animals to that of controls. An increased occurrence of EC cells in the BrdU-labelled zone accounted for the increase in EC cells in the inflamed ileum. Goblet cell numbers were also significantly increased in the inflamed ileum, indicating that cell hyperplasia was not limited to the enteroendocrine cell lineage. This study demonstrates that a small portion of EC cells retain some proliferative capacity; however, hyperplasia associated with ileitis is not attributable to the increased proliferation of EC cells and is not limited to one cell lineage. Therefore, EC cell hyperplasia most probably occurs at the level of the stem cell or recruitment from the progenitor pool.
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http://dx.doi.org/10.1007/s00441-007-0430-6 | DOI Listing |
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