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Intestinal Disease
Research Program, Department of Pathology and Molecular Medicine,
Faculty of Health Sciences, McMaster University, Hamilton, Ontario, L8N
3Z5, Canada
Correspondence to: M H Perdue, Intestinal Disease Research Program, HSC-3N5C, McMaster University, 1200 Main Street West, Hamilton, Ontario, Canada, L8N3Z5. perdue{at}fhs.mcmaster.ca
Accepted for publication 21 November 2000
BACKGROUND AND
AIMS
Stress may be an important factor in
exacerbating inflammatory bowel disease but the underlying mechanism is
unclear. Defective epithelial barrier function may allow uptake of
luminal antigens that stimulate an immune/inflammatory response. Here,
we examined the effect of chronic stress on colonic permeability and
the participation of mast cells in this response.
METHODSMast cell
deficient Ws/Ws rats and +/+ littermate controls were submitted to
water avoidance stress or sham stress (one hour/day) for five days.
Colonic epithelial permeability to a model macromolecular antigen,
horseradish peroxidase, was measured in Ussing chambers. Epithelial and
mast cell morphology was studied by light and electron microscopy.
RESULTSChronic stress
significantly increased macromolecular flux and caused epithelial
mitochondrial swelling in +/+ rats, but not in Ws/Ws rats, compared
with non-stressed controls. Stress increased the number of mucosal mast
cells and the proportion of cells showing signs of activation in +/+
rats. No mast cells or ultrastructural abnormalities of the epithelium
were present in Ws/Ws rats. Increased permeability in +/+ rats
persisted for 72 hours after stress cessation.
CONCLUSIONSChronic
stress causes an epithelial barrier defect and epithelial mitochondrial
damage, in parallel with mucosal mast cell hyperplasia and activation.
The study provides further support for an important role for mast cells
in stress induced colonic mucosal pathophysiology.
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