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S Daum
a Department of
Gastroenterology and Infectious Diseases, Klinikum Benjamin Franklin,
Free University of Berlin, Hindenburgdamm 30, 12200 Berlin, Germany, b Institute of Pathology
Correspondence to: Dr S Daum. Accepted for publication 10 August 1998
Background Keywords:
coeliac disease;
extracellular matrix;
villus
atrophy;
matrix metalloproteinases;
TIMP-1;
collagen I
Extracellular
matrix (ECM) degradation may play a role in villus atrophy in coeliac
disease (CD).
AimsTo compare the
cellular expression of mRNA transcripts for the two major matrix
degrading proteases, matrix metalloproteinase (MMP)-1 and MMP-3, their
inhibitor, tissue inhibitor of metalloproteinases (TIMP)-1, and
procollagen I in the intestinal mucosa of patients with untreated and
treated CD and normal controls.
Patients/MethodsDuodenal
biopsy specimens from ten untreated CD patients, from six of these
after a gluten free diet, and from ten control patients were hybridised
with 35S-labelled RNA probes. The number of positive cells
in the subepithelial region and lamina propria were counted microscopically.
ResultsThe numbers of
cells positive for MMP-1 (p<0.005), MMP-3 (p<0.01), and TIMP-1
(p<0.05) mRNA were higher in the subepithelial region of CD mucosa
than in that from controls. In the lamina propria, only cells positive
for MMP-1 mRNA were increased in CD patients compared with controls
(p<0.01). MMP-1 and MMP-3 mRNA expression returned to normal in CD
patients after treatment with a gluten free diet (p<0.05), while
TIMP-1 mRNA expression remained elevated. The number of procollagen I
mRNA expressing cells did not change. Expression of MMP-1 and MMP-3
mRNA was mainly localised to subepithelial fibroblasts and macrophages.
ConclusionsThe
decreased ratio of collagen I and TIMP-1 mRNA expressing cells to MMP-1
and MMP-3 mRNA expressing cells in untreated CD suggests a shift
towards ECM degradation. ECM degradation by activated subepithelial
fibroblasts and macrophages may be an important mechanism driving
mucosal transformation in CD.
(GUT 1998;44:17-25)
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