title: Inflammatory bowel disease: no association between allele combinations of the interleukin (IL) I beta and IL-I receptor antagonist gene polymorphisms.
abstract: BACKGROUND
  Interleukin 1 (IL-1) and its physiological antagonist interleukin-1 receptor antagonist (IL-1 ra) play a crucial role in the pathogenesis of inflammatory bowel disease. Polymorphisms in the genes coding for these cytokines, the restriction enzyme TaqI polymorphism for IL-1 beta and the variable number of tandem repeats (VNTR) polymorphism for IL-1 ra, have been shown to influence cytokine synthesis in vitro. Recently, an association has been described for distinct allele combinations of these two polymorphisms in patients with ulcerative colitis and with Crohn's disease but not in healthy control subjects.
  
  
  METHODS
  We studied 56 patients with ulcerative colitis, 64 patients with Crohn's disease and 196 healthy control subjects. All were unrelated Caucasians of European ancestry. After polymerase chain reaction (PCR) the amplification products were analysed on agarose gels. For the IL-1 beta polymorphism the PCR product was additionally digested using the restriction enzyme TaqI.
  
  
  RESULTS
  The allele and genotype frequencies as well as the carriage rates of the IL-1 beta TaqI polymorphism in healthy control subjects were in agreement with previous findings in other populations. Allele and genotype frequencies of the IL-1 beta polymorphism were not different in inflammatory bowel disease patients compared with healthy control subjects. Comparing allele combinations of both polymorphisms no association could be identified either within healthy control subjects or in the groups of patients with ulcerative colitis or Crohn's disease.
  
  
  CONCLUSIONS
  Thus, we could not confirm the results of a previous study reporting an association between the IL-1ra and IL-1 beta gene polymorphisms in patients with inflammatory bowel disease.
authors.affiliation: Medizinische Klinik, Klinikum Innenstadt, University of Munich, Germany.
authors.forename: U T
authors.initials: UT
authors.lastname: Hacker
authors.forename: C
authors.initials: C
authors.lastname: Bidlingmaier
authors.forename: M
authors.initials: M
authors.lastname: Gomolka
authors.forename: E
authors.initials: E
authors.lastname: Keller
authors.forename: A
authors.initials: A
authors.lastname: Eigler
authors.forename: G
authors.initials: G
authors.lastname: Hartmann
authors.forename: C
authors.initials: C
authors.lastname: Folwaczny
authors.forename: H
authors.initials: H
authors.lastname: Fricke
authors.forename: E
authors.initials: E
authors.lastname: Albert
authors.forename: K
authors.initials: K
authors.lastname: Loeschke
authors.forename: S
authors.initials: S
authors.lastname: Endres
mesh_terms: D000328:Adult; D000483:Alleles; D001483:Base Sequence; D003093:Colitis, Ulcerative / Q000235:genetics / Q000276:immunology; D003424:Crohn Disease / Q000235:genetics / Q000276:immunology; D017931:DNA Primers / Q000235:genetics; D005260:Female; D006801:Humans; D015212:Inflammatory Bowel Diseases / Q000235:genetics* / Q000276:immunology*; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1 / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D012795:Sialoglycoproteins / Q000235:genetics*
chemical_list: D017931:DNA Primers; C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1; D012795:Sialoglycoproteins