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Myenteric plexus injury and apoptosis in experimental colitis
Lee Boyer1, Mehran Ghoreishi, Valerie Templeman
1British Columbia Research Institute, Vancouver, British Columbia, Canada V6H 3V4.
Autonomic Neuroscience : Basic & Clinical
|December 29, 2004
Summary
Acute colitis causes significant loss of myenteric plexus neurons, partly mediated by neutrophils, leading to impaired colonic motility. This study investigates the neural consequences of intestinal inflammation.
Area of Science:
- Neuroscience
- Gastroenterology
- Immunology
Background:
- Intestinal inflammatory conditions alter the enteric nervous system (ENS).
- Mechanisms of ENS neuronal injury and cell loss in colitis are not fully understood.
Purpose of the Study:
- To investigate the neural consequences of distal colitis.
- To determine the role of neutrophil granulocytes in mediating ENS changes during colitis.
Main Methods:
- Colitis induced in mice using dinitrobenzene sulfonic acid.
- Assessed inflammation via damage scores, myeloperoxidase activity, and histology.
- Examined myenteric plexus using HuC/D and PGP 9.5 immunostaining.
- Investigated neuronal apoptosis using caspase-3 and PARP staining.
Main Results:
- Dinitrobenzene sulfonic acid-induced colitis caused a 42% loss of myenteric plexus neurons, with apoptosis occurring early (0.5-3h).
- No change in overall myenteric plexus density (PGP 9.5), but significant neuronal cell body loss (HuC/D).
- Colitis impaired colonic propulsive function; anti-neutrophil serum partially reduced neuronal loss.
Conclusions:
- Acute colitis leads to significant myenteric plexus neuronal loss.
- Neutrophil granulocytes partially mediate this neuronal injury.
- Colitis-associated neuronal loss contributes to impaired colonic motility.