Enteroendocrine cells and 5-HT availability are altered in mucosa of guinea pigs with TNBS ileitis
Enteroendocrine cells and 5-HT availability are altered in mucosa of guinea pigs with TNBS ileitis
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DOI：
10.1152/ajpgi.00090.2004
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发表时间：
2004-11-01
影响因子：
4.5
通讯作者：
Sharkey, KA
中科院分区：
文献类型：
--
作者：
O'Hara, JR;Ho, WN;Sharkey, KA
肠内分泌细胞作为感觉传感器，释放5-HT和许多参与调节运动、分泌和肠道感觉的肽。粘膜5-HT的作用由5-HT再摄取转运蛋白（SERT）终止。在这项研究中，我们研究了回肠炎导致肠内分泌细胞群和粘膜5-HT可用性变化的假设。通过腔内注射2，4，6-三硝基苯磺酸在豚鼠中诱导回肠炎，并在治疗后3、7和14天进行实验。生长抑素，神经降压素和5-HT免疫反应细胞的数量增加，分别在3和7天的回肠炎，而胆囊收缩素，胰高血糖素样肽-2，葡萄糖依赖性促胰岛素分泌肽，肽YY免疫反应细胞的数量没有显着变化。与基础释放相比，用脱氧胆酸钠对发炎粘膜进行化学刺激显著增加5-HT释放。机械刺激的粘膜加强的效果，在第7天的化学刺激。上皮SERT免疫反应性显着减少，在炎症的时间过程中。因此，肠内分泌细胞群和5-HT可用性的变化可能有助于改变运动和分泌与肠道炎症通过破坏粘膜信号肠神经参与蠕动和分泌反射。
Enteroendocrine cells act as sensory transducers, releasing 5-HT and numerous peptides that are involved in regulating motility, secretion, and gut sensation. The action of mucosal 5-HT is terminated by a 5-HT reuptake transporter (SERT). In this study, we examined the hypothesis that ileitis leads to changes in enteroendocrine cell populations and mucosal 5-HT availability. Ileitis was induced in guinea pigs by intraluminal injection of 2,4,6-trinitrobenzenesulfonic acid and experiments were conducted 3, 7, and 14 days after treatment. The number of somatostatin, neurotensin, and 5-HT-immunoreactive cells increased at 3 and 7 days of ileitis, respectively, whereas no significant changes in the numbers of cholecystokinin, glucagon-like peptide-2, glucose-dependent insulinotropic peptide, and peptide YY-immunoreactive cells were observed. Chemical stimulation of the inflamed mucosa with sodium deoxycholic acid significantly increased 5-HT release compared with basal release. Mechanical stimulation of the mucosa potentiated the effect of the chemical stimuli at day 7. Epithelial SERT immunoreactivity was significantly reduced during the time course of inflammation. Thus changes in enteroendocrine cell populations and 5-HT availability could contribute to the altered motility and secretion associated with intestinal inflammation by disrupting mucosal signaling to enteric nerves involved in peristaltic and secretory reflexes.