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Published on: January 7, 2019
Interstitial cells of cajal and inflammation-induced motor dysfunction in the mouse small intestine
1Intestinal Disease Research Programme, McMaster University, Hamilton, Ontario, Canada.
Insights
Inflammation damages interstitial cells of Cajal (ICC) in the small intestine, disrupting gut motility. Recovery occurs within 60 days, suggesting ICC
Area of Science:
- Gastroenterology
- Cell Biology
- Immunology
Background:
- Interstitial cells of Cajal (ICC) are crucial for regulating gastrointestinal motility.
- Inflammation can lead to motor disorders in the digestive system.
Purpose of the Study:
- To investigate the role of ICC in the development of inflammation-induced gastrointestinal motor dysfunction.
- To examine how inflammation affects ICC structure and function.
Main Methods:
- Studied the effects of Trichinella spiralis infection in mice.
- Assessed electrical pacemaker activity, ICC structure in Auerbach's plexus, and in vivo motor patterns of the small intestine.
Main Results:
- Structural damage to ICC networks and impaired electrical activity were observed during inflammation (days 1-15).
- Abnormal gut motility, including ectopic pacemaker activity and disorganized contractions, occurred.
- All parameters normalized by day 60 post-infection.
Conclusions:
- Inflammation-induced damage to ICC networks disrupts small intestinal motor patterns.
- ICC play a significant role in inflammation-related gastrointestinal motor disturbances.
- The findings highlight the dynamic nature of ICC network recovery post-inflammation.
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.
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