title: CD14 expression on monocytes and soluble CD14 plasma levels in correlation to the promotor polymorphism of the endotoxin receptor CD14 gene in patients with inactive Crohn's disease.
abstract: OBJECTIVE
  The association of the single nucleotide polymorphism in the promotor of the lipopolysaccharide receptor CD14 gene (T/C at position -159) with Crohn's disease has recently been demonstrated. This CD14 polymorphism is a potential predisposition factor responsible for inter-individual differing inflammatory reactions involving the CD14 receptor. We studied the correlation between the CD14 genotype (CC, CT, TT) and the membrane-bound CD14 monocyte expression and soluble CD14 in patients with inactive Crohn's disease.
  
  
  METHODS
  In 23 patients and 29 healthy volunteers the membrane-bound CD14 density on unstimulated monocytes and soluble CD14 plasma levels were examined using quantitative flow cytometry and enzyme-linked immunosorbent assay.
  
  
  RESULTS
  In normal controls membrane-bound CD14 monocyte density did not differ significantly between the genotypes CC, CT, or TT. In contrast, patients with inactive Crohn's disease and genotype TT showed a significantly lower membrane-bound CD14 density on monocytes compared to patients with genotype CC. Soluble CD14 plasma levels were significantly higher in patients with inactive Crohn's disease compared to the same genotype of healthy controls, but there was no significant difference between the genotypes CC, CT, and TT.
  
  
  CONCLUSIONS
  Our data show that the membrane-bound CD14 monocyte expression and the soluble CD14 plasma levels in patients with inactive Crohn's disease completely differ from that in healthy individuals. In order to develop individualized therapy strategies further studies should be carried out to evaluate whether the TT genotype is associated with differences in the clinical course of Crohn's disease and in the response to antibacterial treatment.
authors.affiliation: Department of Gastroenterology, University Hospital Bergmannsheil, Bochum, Germany. thomas.griga@ruhr-uni-bochum.de
authors.forename: Thomas
authors.initials: T
authors.lastname: Griga
authors.forename: Wolfram
authors.initials: W
authors.lastname: Klein
authors.forename: Jorg T
authors.initials: JT
authors.lastname: Epplen
authors.forename: Ute
authors.initials: U
authors.lastname: Hebler
authors.forename: Axel
authors.initials: A
authors.lastname: Stachon
authors.forename: Burkard
authors.initials: B
authors.lastname: May
mesh_terms: D000328:Adult; D003424:Crohn Disease / Q000175:diagnosis / Q000235:genetics*; D004198:Disease Susceptibility / Q000175:diagnosis; D005260:Female; D015870:Gene Expression; D005838:Genotype; D006801:Humans; D018950:Lipopolysaccharide Receptors / Q000097:blood* / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000378:metabolism*; D011110:Polymorphism, Genetic; D011401:Promoter Regions, Genetic / Q000235:genetics*; D011971:Receptors, Immunologic / Q000235:genetics*; D013223:Statistics as Topic
chemical_list: D018950:Lipopolysaccharide Receptors; D011971:Receptors, Immunologic; C048071:endotoxin receptor