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Equine veterinary journal2019; 52(2); 298-304; doi: 10.1111/evj.13160

Myenteric networks of interstitial cells of Cajal are reduced in horses with inflammatory bowel disease.

Abstract: Inflammatory bowel disease (IBD) is a well-recognised but poorly understood disease complex in the horse. Clinical signs may vary but often include weight loss, diarrhoea and colic. The effect this disease process may have on the gastrointestinal pacemaker cells (the interstitial cells of Cajal), enteric neurons and glial cells has not been previously evaluated in the horse. Objective: To compare the density of the interstitial cells of Cajal (ICC), enteric neurons and glial cells in horses with IBD to those of normal horses using immunohistochemical markers. Methods: Retrospective, quantitative immunohistochemical study. Methods: Ileal samples were collected during post-mortem examinations from 14 horses with a clinical and histopathological diagnosis of IBD and from eight normal controls. All horses were Standardbreds 1-15 years of age. Six of the IBD cases had eosinophilic gastroenteritis (EG) while the remaining eight had granulomatous enteritis (GE). Tissue sections were labelled with anti-CD117 (c-Kit), anti-TMEM16 (TMEM16), anti-protein gene product (PGP9.5) and anti-glial fibrillary acidic protein (GFAP) using standard immunohistochemical labelling techniques. Image analysis was performed to quantify the presence of ICC (CD117, TMEM16) as well as neuronal (PGP9.5) and enteroglial (GFAP) networks. Results: Interstitial cells of Cajal networks were significantly reduced in the myenteric plexus (MP) region in IBD horses compared with the controls for both markers (P<0.05). There was no significant difference in the density of the neuronal or glial cell markers between the two groups (P>0.05). Conclusions: The number of horses included in the study. Conclusions: Disruption to ICC networks may contribute to the clinical signs of colic in some horses with IBD. Further studies are needed to establish the pathophysiological mechanisms involved and the functional effects of the reduced ICC networks.
© 2019 The Authors. Equine Veterinary Journal published by John Wiley & Sons Ltd on behalf of EVJ Ltd.
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Publication Date: 2019-09-05 PubMed ID: 31397916DOI: 10.1111/evj.13160Google Scholar: Lookup
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Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

The research examines the impact of Inflammatory Bowel Disease (IBD) in horses on gastrointestinal pacemaker cells (interstitial cells of Cajal), enteric neurons, and glial cells. Results reveal a significant reduction of interstitial cells of Cajal in affected horses, potentially contributing to clinical symptoms like colic.

Objective of the Study

  • The study aimed to examine the density of interstitial cells of Cajal (ICCs), enteric neurons, and glial cells in horses with IBD and compare it with normal horses. This was achieved using specific immunohistochemical markers.

Research Methodology

  • As a retrospective, quantitative immunohistochemical study, it utilized ileal samples taken during post-mortem examinations of 14 horses diagnosed with IBD and 8 control horses.
  • The IBD cases consisted of six horses with eosinophilic gastroenteritis (EG) and eight with granulomatous enteritis (GE).
  • The selected tissue samples were then labelled with anti-CD117 (c-Kit), anti-TMEM16 (TMEM16), protein gene product (PGP9.5), and anti-glial fibrillary acidic protein (GFAP), following standard immunohistochemical protocols.
  • Image analysis was then utilized to quantify the presence of ICCs (using CD117 and TMEM16), as well as neuronal (PGP9.5) and enteroglial (GFAP) networks.

Key Findings

  • The results showed a significant decrease in the networks of the interstitial cells of Cajal located in the myenteric plexus region of horses with IBD when compared with the control horses.
  • In contrast, the density of neuronal or glial cell markers did not show a significant difference between the two groups.

Conclusions and Implications

  • The findings suggest that disruptions to the ICC networks could be a contributing factor to symptoms such as colic in horses suffering from IBD.
  • However, the exact pathophysiological mechanisms involved in this process, and the functional effects of reduced ICC networks, still need to be established through further studies.

Cite This Article

APA
Fintl C, Lindberg R, McL Press C. (2019). Myenteric networks of interstitial cells of Cajal are reduced in horses with inflammatory bowel disease. Equine Vet J, 52(2), 298-304. https://doi.org/10.1111/evj.13160

Publication

Equine veterinary journal
ISSN: 2042-3306
NlmUniqueID: 0173320
Country: United States
Language: English
Volume: 52
Issue: 2
Pages: 298-304

Researcher Affiliations

Fintl, C
  • Norwegian University of Life Sciences, Oslo, Norway.
Lindberg, R
  • Swedish University of Agricultural Sciences, Uppsala, Sweden.
McL Press, C
  • Norwegian University of Life Sciences, Oslo, Norway.

MeSH Terms

  • Animals
  • Colic / veterinary
  • Horse Diseases
  • Horses
  • Inflammatory Bowel Diseases / veterinary
  • Interstitial Cells of Cajal
  • Myenteric Plexus
  • Retrospective Studies

Grant Funding

  • Agricultural Agreement Research Fund
  • Norsk Rikstoto
  • Research Council of Norway
  • 41519 / Norwegian/Swedish research collaboration

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Citations

This article has been cited 3 times.
  1. Li J, Liu F, Mo K, Ni H, Yin Y. Effects of weaning on intestinal longitudinal muscle-myenteric plexus function in piglets. Sci China Life Sci 2024 Feb;67(2):379-390.
    doi: 10.1007/s11427-022-2391-xpubmed: 37824029google scholar: lookup
  2. Kaji N, Hori M. Interstitial cells of Cajal in gastrointestinal inflammatory diseases. J Smooth Muscle Res 2023;59:1-13.
    doi: 10.1540/jsmr.59.1pubmed: 36792171google scholar: lookup
  3. Erwin SJ, Blikslager AT, Ziegler AL. Age-Dependent Intestinal Repair: Implications for Foals with Severe Colic. Animals (Basel) 2021 Nov 23;11(12).
    doi: 10.3390/ani11123337pubmed: 34944114google scholar: lookup
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