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

被引:131
作者
Der, T
Bercik, P
Donnelly, G
Jackson, T
Berezin, I
Collins, SM
Huizinga, JD
机构
[1] McMaster Univ, Intestinal Dis Res Programme, Hamilton, ON, Canada
[2] McMaster Univ, Dept Med, Hamilton, ON, Canada
基金
英国医学研究理事会;
关键词
D O I
10.1053/gast.2000.20221
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
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 stow 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.
引用
收藏
页码:1590 / 1599
页数:10
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