title: Expression of 5-lipoxygenase mRNA is unchanged in the colon of patients with active inflammatory bowel disease.
abstract: BACKGROUND
  In inflammatory bowel disease (IBD) the disease activity correlates with colonic concentrations of leukotrienes (LTs). The enzyme 5-lipoxygenase (5-LO) is responsible for the enzymatic production of LTs. It has previously been demonstrated in experimental models of inflammation, that 5-LO is activated through intracellular translocation of the pre-formed enzyme, and increased constitutive activation of 5-LO has been demonstrated in idiopathic pulmonary fibrosis. The objective of the present study was to investigate whether de novo synthesis of 5-LO is increased in patients with quiescent IBD, or is induced during acute exacerbations of IBD.
  
  
  METHODS
  Sixty-one individuals were included in the study. Twenty-eight had ulcerative colitis (UC), 21 had Crohn's disease (CD), and 12 were healthy controls. A standard rigid rectoscopy was performed in all individuals. The degree of inflammation was assessed using a semi-quantitative scale. A mucosal biopsy was taken from the most inflamed area as judged macroscopically. mRNA for 5-LO was detected using a RT-PCR technique, and the assay applied was evaluated by control experiments.
  
  
  RESULTS
  The expression of mRNA for 5-LO in colonic biopsies was similar in IBD patients with quiescent disease and healthy controls. When grouped according to endoscopically assessed disease activity the fraction of patients demonstrating 5-LO mRNA in colonic biopsies showed no significant change (p > 0,6; chi2 -test for trend).
  
  
  CONCLUSIONS
  This study demonstrates no significant relationship between endoscopically assessed disease activity and relative presence of mRNA for 5-LO in colonic biopsies. Thus, there is no evidence of increased expression of 5-LO mRNA in either quiescent or active stages of IBD.
authors.affiliation: Department of Medical Gastroenterology C, Herlev Hospital, University of Copenhagen, Denmark.
authors.forename: J
authors.initials: J
authors.lastname: Hendel
authors.forename: I
authors.initials: I
authors.lastname: Ahnfelt-Rønne
authors.forename: O H
authors.initials: OH
authors.lastname: Nielsen
mesh_terms: D000328:Adult; D003106:Colon / Q000201:enzymology*; D003108:Colonic Diseases / Q000201:enzymology / Q000235:genetics; D051546:Cyclooxygenase 2; D005260:Female; D015971:Gene Expression Regulation, Enzymologic; D006801:Humans; D007249:Inflammation / Q000201:enzymology / Q000235:genetics; D015212:Inflammatory Bowel Diseases / Q000201:enzymology* / Q000235:genetics; D007527:Isoenzymes / Q000235:genetics; D008084:Lipoxygenase / Q000235:genetics*; D008297:Male; D008565:Membrane Proteins; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D011451:Prostaglandin-Endoperoxide Synthases / Q000235:genetics; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism*
chemical_list: D007527:Isoenzymes; D008565:Membrane Proteins; D012333:RNA, Messenger; D008084:Lipoxygenase; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases