title: Increased expression of IL-16 in inflammatory bowel disease.
abstract: 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-1beta, IL-6, IL-15, and tumour necrosis factor alpha (TNF-alpha) in human monocytes.
  
  
  OBJECTIVE
  To examine if IL-16 expression is increased in IBD patients compared with healthy controls.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Ist Department of Medicine, Christian-Albrechts-University, Schittenhelmstrasse 12, D-24105 Kiel, Germany. s.seegert@mucosa.de
authors.forename: D
authors.initials: D
authors.lastname: Seegert
authors.forename: P
authors.initials: P
authors.lastname: Rosenstiel
authors.forename: H
authors.initials: H
authors.lastname: Pfahler
authors.forename: P
authors.initials: P
authors.lastname: Pfefferkorn
authors.forename: S
authors.initials: S
authors.lastname: Nikolaus
authors.forename: S
authors.initials: S
authors.lastname: Schreiber
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001706:Biopsy; D015153:Blotting, Western; D016022:Case-Control Studies; D020169:Caspases / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D004804:Eosinophils / Q000378:metabolism; D005260:Female; D015870:Gene Expression; D006801:Humans; D015212:Inflammatory Bowel Diseases / Q000378:metabolism* / Q000473:pathology; D019410:Interleukin-16 / Q000235:genetics / Q000378:metabolism*; D007413:Intestinal Mucosa / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D012333:RNA, Messenger / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015854:Up-Regulation
chemical_list: D019410:Interleukin-16; D012333:RNA, Messenger; D020169:Caspases