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小鼠小肠中的卡哈尔间质细胞与炎症诱导的运动功能障碍

Interstitial cells of cajal and inflammation-induced motor dysfunction in the mouse small intestine.

作者信息

Der T, Bercik P, Donnelly G, Jackson T, Berezin I, Collins S M, Huizinga J D

机构信息

Intestinal Disease Research Programme, McMaster University, Hamilton, Ontario, Canada.

出版信息

Gastroenterology. 2000 Dec;119(6):1590-9. doi: 10.1053/gast.2000.20221.

DOI:10.1053/gast.2000.20221
PMID:11113080
Abstract

BACKGROUND & AIMS: Interstitial cells of Cajal (ICC) play an important role in the control of gastrointestinal motility. We aimed to determine a potential role for ICC in the pathophysiology of inflammation-induced motor disorders.

METHODS

Effects of Trichinella spiralis infection on electrical pacemaker activity, the structure of ICC associated with Auerbach's plexus, and in vivo motor patterns were studied in the mouse small intestine.

RESULTS

Between days 1 and 15 after infection, structural damage occurred in the network of ICC, particularly in the processes connecting ICC to each other and to smooth muscle cells. This was associated with desynchronization of electrical pacemaker activity. Abnormal slow wave activity occurred, including doubling of frequency and electrical quiescence, leading to the development of ectopic pacemaker activity in vivo. In vivo motor patterns in the small intestine changed from consistent peristaltic contractile activity in control animals to periods of quiescence alternating with both orally and aborally propagating contractile activity in the presence of inflammation. Sixty days after infection, all parameters studied had returned to normal values.

CONCLUSIONS

Inflammation-induced alterations in the network of ICC of the small intestine associated with Auerbach's plexus lead to disorganization of motor patterns. Because of the strong temporal correlation between damage to the ICC network, electrical uncoupling, the appearance of ectopic pacemaker activity, and the occurrence of retrograde peristalsis, it is concluded that ICC can play a major role in inflammation-induced motor disturbances.

摘要

背景与目的

Cajal间质细胞(ICC)在胃肠动力控制中发挥重要作用。我们旨在确定ICC在炎症诱导的运动障碍病理生理学中的潜在作用。

方法

研究旋毛虫感染对小鼠小肠电起搏活动、与奥尔巴赫神经丛相关的ICC结构及体内运动模式的影响。

结果

感染后第1天至第15天,ICC网络出现结构损伤,尤其是ICC相互连接以及与平滑肌细胞连接的突起。这与电起搏活动的去同步化有关。出现异常慢波活动,包括频率加倍和电静止,导致体内异位起搏活动的发生。小肠的体内运动模式从对照动物中一致的蠕动收缩活动转变为在炎症存在时静止期与向口腔和向肛门传播的收缩活动交替出现。感染60天后,所有研究参数均恢复至正常水平。

结论

与奥尔巴赫神经丛相关的小肠ICC网络炎症诱导的改变导致运动模式紊乱。由于ICC网络损伤、电去耦联、异位起搏活动的出现和逆行蠕动的发生之间存在强烈的时间相关性,得出结论:ICC在炎症诱导的运动障碍中可发挥主要作用。

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