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Gastrointestinal Motility Monitor GIMM
Published on: December 1, 2010
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Glioplasticity in irritable bowel syndrome
N L Lilli1,2, L Quénéhervé1,2, S Haddara1,2
1Université de Nantes, INSERM, IMAD, The enteric nervous system in gut and brain disorders, Université Bretagne Loire, Nantes, France.
Neurogastroenterology and Motility
|October 14, 2017
Summary
Irritable bowel syndrome (IBS) involves changes in enteric glial cells (EGCs). Histamine acting on H1 receptors alters EGC function, potentially contributing to IBS pain and bloating.
Area of Science:
- Gastroenterology
- Neuroscience
- Cell Biology
Background:
- Irritable bowel syndrome (IBS) is associated with cellular changes in the gut lining.
- Enteric glial cells (EGCs) are crucial for gut function and may be altered in IBS.
Purpose of the Study:
- To investigate alterations in EGCs in IBS patients.
- To identify factors and mechanisms responsible for EGC changes in IBS.
Main Methods:
- Analyzing colonic biopsies from IBS patients and healthy controls for S100β and GFAP expression.
- Incubating cultured rat EGCs with IBS patient mucosal supernatants to assess proliferation and Ca2+ response.
- Investigating the role of histamine and histamine 1-receptor (H1R) in supernatant-induced EGC effects.
Main Results:
- Reduced S100β expression in IBS patient biopsies correlated with pain and bloating.
- IBS supernatants altered EGC proliferation and Ca2+ response to ATP.
- Histamine acting via H1R mediated some supernatant effects on EGCs, and connexin-43 mRNA expression was reduced.
Conclusions:
- EGCs are altered in IBS, influenced by mucosal soluble factors.
- Histamine-mediated pathways involving H1R contribute to altered EGC Ca2+ signaling in IBS.
- These EGC changes may play a role in IBS pathophysiology, pain, and bloating perception.
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