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a Ist
Department of Medicine, Christian-Albrechts- University Kiel, Germany, b Institute of
Anatomy, Christian-Albrechts- University Kiel, Germany
Correspondence to: Dr D Seegert, Ist Department of Medicine,
Christian-Albrechts-University, Schittenhelmstra
e 12, D-24105 Kiel,
Germany.
d.seegert{at}mucosa.de
Accepted for publication 22 August 2000
BACKGROUND
Inflammatory
bowel disease (IBD) is characterised by infiltration of inflamed
mucosal regions with CD4+ T lymphocytes and other
mononuclear cells. Interleukin (IL)-16 exerts a strong
chemoattractant activity on CD4+ cells. Moreover, IL-16
activates expression and production of proinflammatory cytokines such
as IL-1, IL-6, IL-15, and tumour necrosis factor 
(TNF-) in
human monocytes.
AIMTo examine if
IL-16 expression is increased in IBD patients compared with healthy controls.
METHODSTwenty one
patients with IBD (10 with ulcerative colitis (UC), 11 with
Crohn's disease (CD)), seven disease specificity controls (DSC),
and seven healthy controls were studied. Biopsies were taken during
colonoscopies and IL-16 mRNA as well as protein expression were
investigated by reverse transcriptase-polymerase chain reaction, ELISA,
western blot, and immunohistochemistry.
RESULTSIL-16 mRNA and
protein expression in the colonic mucosa of IBD patients were increased
twofold compared with healthy controls, DSC, or IBD patients under
steroid treatment. Most of the detected IL-16 protein was in its
bioactive 17 kDa form and was predominantly expressed in eosinophils.
Increased IL-16 expression in UC patients appeared to be mainly
restricted to the inflamed regions of the colonic mucosa. Levels of
caspase 3, which processes the 68 kDa IL-16 precursor molecule into the
biological active 17 kDa form, were not increased.
CONCLUSIONSOur
results provide evidence that IL-16 expression is significantly
increased in the inflamed colonic mucosa of IBD patients but not in
control individuals, DSC, or patients under steroid treatment.
Therefore, upregulation of IL-16 expression seems to be specific for
chronic intestinal inflammation and could lead to increased secretion
of other proinflammatory cytokines in IBD.
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