title: Comparison of glucocorticoid and cysteinyl leukotriene receptor antagonist treatments in an experimental model of chronic airway inflammation in guinea-pigs.
abstract: BACKGROUND
  Leukotriene receptor antagonists have been demonstrated in several studies to possess bronchodilating and anti-inflammatory properties in asthma. However, there are few experimental studies performed to compare the effects of anti-leukotrienes and glucocorticoids, most used anti-inflammatory agents in asthma. In the present study, we evaluated the effects of treatment with dexamethasone or montelukast on eosinophil and mononuclear cell recruitment in an experimental model of allergen-induced chronic airway inflammation in guinea-pigs (GP).
  
  
  METHODS
  GP were submitted to increasing concentrations of aerosols of ovalbumin (OVA) twice a week for 4 weeks. After 2 weeks, animals were treated daily with dexamethasone, montelukast or saline solution. After this period, GP were anaesthetized, tracheostomized, mechanically ventilated and challenged with OVA aerosol.
  
  
  RESULTS
  Maximal changes of respiratory system resistance and elastance induced by OVA challenge were attenuated by dexamethasone (P<0.001), but not by montelukast treatment. Neither dexamethasone nor montelukast significantly influenced bronchial oedema formation. Dexamethasone but not montelukast induced a decrease in mononuclear cells in airways (P<0.001). Eosinophil infiltration in the bronchial wall was reduced by both dexamethasone and montelukast (P<0.005). Only dexamethasone treatment reduced the levels of exhaled nitric oxide (P<0.025).
  
  
  CONCLUSIONS
  Although leukotriene receptor antagonist treatment reduces eosinophil accumulation induced by multiple antigen challenges, glucocorticoid treatment attenuates both eosinophil and mononuclear cell infiltration.
authors.affiliation: Department of Medicine, School of Medicine, University of São Paulo, São Paulo, Brazil.
authors.forename: E A
authors.initials: EA
authors.lastname: Leick-Maldonado
authors.forename: F U
authors.initials: FU
authors.lastname: Kay
authors.forename: M C
authors.initials: MC
authors.lastname: Leonhardt
authors.forename: D I
authors.initials: DI
authors.lastname: Kasahara
authors.forename: C M
authors.initials: CM
authors.lastname: Prado
authors.forename: F T
authors.initials: FT
authors.lastname: Fernandes
authors.forename: M A
authors.initials: MA
authors.lastname: Martins
authors.forename: I F L C
authors.initials: IF
authors.lastname: Tibério
mesh_terms: D000085:Acetates / Q000627:therapeutic use*; D000818:Animals; D001249:Asthma / Q000188:drug therapy* / Q000276:immunology; D002908:Chronic Disease; D003521:Cyclopropanes; D003907:Dexamethasone / Q000627:therapeutic use*; D004804:Eosinophils / Q000276:immunology; D005938:Glucocorticoids / Q000627:therapeutic use*; D006168:Guinea Pigs; D007958:Leukocyte Count; D020024:Leukotriene Antagonists / Q000627:therapeutic use*; D008168:Lung / Q000276:immunology; D008297:Male; D011804:Quinolines / Q000627:therapeutic use*; D013440:Sulfides
chemical_list: D000085:Acetates; D003521:Cyclopropanes; D005938:Glucocorticoids; D020024:Leukotriene Antagonists; D011804:Quinolines; D013440:Sulfides; D003907:Dexamethasone; C093875:montelukast