title: Increased prostaglandin E2 levels in the airway of patients with eosinophilic bronchitis.
abstract: BACKGROUND
  Eosinophilic bronchitis is a common cause of chronic cough, which like asthma is characterized by sputum eosinophilia, but unlike asthma there is no variable airflow obstruction or airway hyperresponsiveness. We tested the hypothesis that the different airway function in patients with eosinophilic bronchitis and asthma could be caused by an imbalance in the production of bronchoconstrictor (LTC(4)) and bronchoprotective (prostaglandin E(2); PGE(2)) lipid mediators.
  
  
  METHODS
  We measured cytokines levels, proinflammatory mediators and eicosanoids concentration in sputum from 13 subjects with nonasthmatic eosinophilic bronchitis, 13 subjects with asthma, and 11 healthy control subjects. Cytokines mRNA levels were measured by real time PCR, proinflammatory mediators, PGE(2), and LTC(4) were measured by enzyme immunoassays.
  
  
  RESULTS
  The median sputum eosinophil count was not statistically different in patients with asthma (7.95%) and eosinophilic bronchitis (15.29%). The levels of mRNA specific to interleukin-5 (IL-5), IL-4, IL-10, IL-13, interferon gamma (IFN-gamma), IL-2, vascular endothelial growth factor and transforming growth factor beta were similar in both conditions. In addition, no differences were found between asthma and eosinophilic bronchitis in proinflammatory cytokines, such as IL-8, IFN-gamma and tumor necrosis factor alpha (TNF-alpha) levels. Sputum cysteinyl-leukotrienes concentration was raised both in eosinophilic bronchitis and asthma patients. We found that induced sputum PGE(2) concentrations were significantly increased in subjects with eosinophilic bronchitis (838.3 +/- 612 pg/ml) when compared with asthmatic (7.54 +/- 2.14 pg/ml) and healthy subjects (4 +/- 1.3 pg/ml).
  
  
  CONCLUSIONS
  This data suggest that the difference in airway function observed in subjects with eosinophilic bronchitis and asthma could be due to differences in PGE(2) production in the airways.
authors.affiliation: Immunology Department Fundación Jiménez Díaz Capio, CIBERES (ISCIII), Madrid, Spain.
authors.forename: B
authors.initials: B
authors.lastname: Sastre
authors.forename: M
authors.initials: M
authors.lastname: Fernández-Nieto
authors.forename: R
authors.initials: R
authors.lastname: Mollá
authors.forename: E
authors.initials: E
authors.lastname: López
authors.forename: C
authors.initials: C
authors.lastname: Lahoz
authors.forename: J
authors.initials: J
authors.lastname: Sastre
authors.forename: V
authors.initials: V
authors.lastname: del Pozo
authors.forename: S
authors.initials: S
authors.lastname: Quirce
mesh_terms: D000328:Adult; D000368:Aged; D001249:Asthma / Q000276:immunology* / Q000503:physiopathology; D001991:Bronchitis / Q000276:immunology* / Q000503:physiopathology; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D016022:Case-Control Studies; D016207:Cytokines / Q000378:metabolism; D015232:Dinoprostone / Q000032:analysis* / Q000276:immunology; D004797:Enzyme-Linked Immunosorbent Assay; D004802:Eosinophilia / Q000276:immunology* / Q000503:physiopathology; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D011336:Probability; D011379:Prognosis; D012333:RNA, Messenger / Q000032:analysis; D012016:Reference Values; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D013183:Sputum / Q000737:chemistry; D018709:Statistics, Nonparametric
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D012333:RNA, Messenger; D015232:Dinoprostone