title: Cysteinyl leukotriene 1 receptor expression associated with bronchial inflammation in severe exacerbations of COPD.
abstract: BACKGROUND
  Cysteinyl leukotriene 1 (CysLT1) receptor expression is known to be increased in the airway mucosa of patients with asthma, especially during exacerbations; however, nothing is known of its expression in COPD.
  
  
  METHODS
  We applied immunohistochemistry and in situ hybridization to endobronchial biopsies to determine inflammatory cell CysLT1 receptor protein and mRNA expression in the following: (1) 15 nonsmoker control subjects (NSC), (2) 16 smokers with moderate to severe COPD in its stable phase (S-COPD), and (3) 15 smokers with COPD hospitalized for a severe exacerbation (SE-COPD).
  
  
  RESULTS
  The total number of bronchial mucosal inflammatory cells (CD45+) and those expressing CysLT1 receptor protein were significantly greater in SE-COPD (CysLT1 receptor protein: median [range] = 139 [31-634]) as compared with S-COPD (32 [6-114]) or NSC (16 [4-66]) (P < .001 for both). CysLT1 receptor gene expression showed similar differences. A greater proportion of CD451 cells expressed CysLT1 receptor protein in SE-COPD (median [range] = 22% [8-81]) compared with S-COPD (10% [4-32]) (P < .03) or NSC (7% [1-19]) (P < .002). In SE-COPD, the relative frequencies of CysLT1 receptor-expressing cells were as follows: tryptase1 mast cells > CD681 monocytes/macrophage > neutrophils > CD201 B lymphocytes = EG21 eosinophils. Moreover, there were positive correlations between the numbers of cells expressing CysLT1 receptor protein and the numbers of CD451 cells (r = 0.78; P < .003) and tryptase1 mast cells (r = 0.62; P < .02).
  
  
  CONCLUSIONS
  Bronchial mucosal CysLT1 receptor-positive inflammatory cells are present in the bronchial mucosa in COPD in greatest number in those experiencing a severe exacerbation.
authors.affiliation: Lung Pathology Unit, Department of Respiratory Medicine, Imperial College London, London, England.
authors.forename: Jie
authors.initials: J
authors.lastname: Zhu
authors.affiliation: Department of Medicine, Baylor College of Medicine, Ben Taub General Hospital, Houston, TX.
authors.forename: Venkata
authors.initials: V
authors.lastname: Bandi
authors.affiliation: Lung Pathology Unit, Department of Respiratory Medicine, Imperial College London, London, England.
authors.forename: Shengyang
authors.initials: S
authors.lastname: Qiu
authors.affiliation: Department of Pharmacology, Merck & Co Inc, West Point, PA.
authors.forename: David J
authors.initials: DJ
authors.lastname: Figueroa
authors.affiliation: Department of Pharmacology, Merck & Co Inc, West Point, PA.
authors.forename: Jilly F
authors.initials: JF
authors.lastname: Evans
authors.affiliation: Department of Respiratory Medicine, Barts and The London Hospital, London, England.
authors.forename: Neil
authors.initials: N
authors.lastname: Barnes
authors.affiliation: Department of Medicine, Baylor College of Medicine, Ben Taub General Hospital, Houston, TX.
authors.forename: Kay K
authors.initials: KK
authors.lastname: Guntupalli
authors.affiliation: Lung Pathology Unit, Department of Respiratory Medicine, Imperial College London, London, England. Electronic address: p.jeffery@imperial.ac.uk.
authors.forename: Peter K
authors.initials: PK
authors.lastname: Jeffery
mesh_terms: D000328:Adult; D000368:Aged; D001980:Bronchi / Q000378:metabolism / Q000473:pathology*; D016022:Case-Control Studies; D015331:Cohort Studies; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D029424:Pulmonary Disease, Chronic Obstructive / Q000209:etiology / Q000378:metabolism* / Q000473:pathology*; D012333:RNA, Messenger / Q000378:metabolism*; D018077:Receptors, Leukotriene / Q000235:genetics* / Q000378:metabolism*; D020545:Respiratory Mucosa / Q000378:metabolism / Q000473:pathology; D012907:Smoking / Q000235:genetics / Q000378:metabolism / Q000473:pathology
chemical_list: D012333:RNA, Messenger; D018077:Receptors, Leukotriene; C083169:leukotriene D4 receptor