Increased expression of IL-16 in inflammatory bowel disease.

Authors:
D Seegert, P Rosenstiel, H Pfahler, P Pfefferkorn, S Nikolaus, S Schreiber
Year of publication:
2001
Volume:
48
Issue:
3
Issn:
0017-5749
Journal title abbreviated:
GUT
Journal title long:
Gut : journal of the British Society of Gastroenterology
Impact factor:
14.921
Abstract:
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-1beta, IL-6, IL-15, and tumour necrosis factor alpha (TNF-alpha) in human monocytes.To examine if IL-16 expression is increased in IBD patients compared with healthy controls.Twenty 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.IL-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.Our 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.