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首页> 外文期刊>American Journal of Physiology >Stress stimulates transepithelial macromolecular uptake in rat jejunum.
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Stress stimulates transepithelial macromolecular uptake in rat jejunum.

机译：应激刺激大鼠空肠中上皮的大分子摄取。

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摘要

Evidence suggests that stress may be a contributing factor in intestinal inflammatory disease; however, the involved mechanisms have not been elucidated. We previously reported that acute stress alters epithelial physiology of rat intestine. In this study, we documented stress-induced macromolecular transport across intestinal epithelium. After exposure of Wistar-Kyoto rats to acute restraint stress, transport of a model protein, horseradish peroxidase (HRP), was assessed in isolated segments of jejunum. The flux of intact HRP was significantly enhanced across intestine from stressed rats compared with controls. Electron microscopy revealed HRP-containing endosomes within enterocytes, goblet cells, and Paneth cells of stressed rats. The number and area of HRP endosomes within enterocytes were found to be significantly increased by stress. HRP was also visualized in paracellular spaces between adjacent epithelial cells only in intestine from stressed rats. Atropine treatment of rats prevented the stress-induced abnormalities of protein transport. Our results suggest that stress, via a mechanism that involves release of acetylcholine, causes epithelial dysfunction that includes enhanced uptake of macromolecular protein antigens. We speculate that immune reactions to such foreign proteins may initiate or exacerbate inflammation.
机译：有证据表明，压力可能是肠道炎性疾病的一个促成因素。但是，所涉及的机制尚未阐明。我们先前曾报道急性应激会改变大鼠肠的上皮生理。在这项研究中，我们记录了应力诱导的大分子跨肠上皮运输。将Wistar-Kyoto大鼠暴露于急性束缚压力后，评估了空肠孤立段中模型蛋白辣根过氧化物酶（HRP）的转运。与对照组相比，压力大鼠的肠道中完整HRP的通量显着提高。电子显微镜显示应激大鼠肠细胞，杯状细胞和Paneth细胞内含HRP的内体。发现肠内细胞中HRP内体的数量和面积因压力而显着增加。还仅在应激大鼠的肠中在相邻上皮细胞之间的旁细胞间隙中观察到了HRP。阿托品对大鼠的治疗可预防应激引起的蛋白质转运异常。我们的结果表明，应激通过一种涉及乙酰胆碱释放的机制引起上皮功能障碍，其中包括大分子蛋白质抗原的摄取增加。我们推测对此类外源蛋白质的免疫反应可能引发或加剧炎症。

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