title: Comparison of acute inflammatory and chronic structural asthma-like responses between C57BL/6 and BALB/c mice.
abstract: BACKGROUND
  The interactions between airway responsiveness, structural remodelling and inflammation in allergic asthma remain poorly understood. Prolonged challenge with inhaled allergen is necessary to replicate many of the features of airway wall remodelling in mice. In both mice and humans, genetic differences can have a profound influence on allergy, inflammation, airway responsiveness and structural changes.
  
  
  METHODS
  The aim of this study was to provide a comparative analysis of allergen-induced airway changes in sensitized BALB/c and C57BL/6 mice that were exposed to inhaled allergen for 2 ('acute'), 6 or 9 weeks ('chronic'). Inflammation, remodelling and responsiveness were analyzed.
  
  
  RESULTS
  Both strains developed a Th-2-driven airway inflammation with allergen-specific IgE, airway eosinophilia and goblet cell hyperplasia upon 2 weeks of allergen inhalation. This was accompanied by a significant increase in airway smooth muscle mass and hyperresponsiveness in BALB/c but not in C57BL/6 mice. However, airway eosinophilia was more pronounced in the C57BL/6 strain. Chronic allergen exposure (6 or 9 weeks) resulted in an increase in airway smooth muscle mass as well as subepithelial collagen and fibronectin deposition in both strains. The emergence of these structural changes paralleled the disappearance of inflammation in both C57BL/6 and BALB/c mice and loss of hyperresponsiveness in the BALB/c strain. TGF-beta(1 )was accordingly elevated in both strains.
  
  
  CONCLUSIONS
  Airway inflammation, remodelling and hyperresponsiveness are closely intertwined processes. Genetic background influences several aspects of the acute allergic phenotype. Chronic allergen exposure induces a marked airway remodelling that parallels a decreased inflammation, which was largely comparable between the two strains.
authors.affiliation: Department of Respiratory Medicine, Ghent University, Ghent, Belgium. chris.vanhove@UGent.be
authors.forename: Chris L
authors.initials: CL
authors.lastname: Van Hove
authors.forename: Tania
authors.initials: T
authors.lastname: Maes
authors.forename: Didier D
authors.initials: DD
authors.lastname: Cataldo
authors.forename: Maud M
authors.initials: MM
authors.lastname: Guéders
authors.forename: Els
authors.initials: E
authors.lastname: Palmans
authors.forename: Guy F
authors.initials: GF
authors.lastname: Joos
authors.forename: Kurt G
authors.initials: KG
authors.lastname: Tournoy
mesh_terms: D000208:Acute Disease; D000280:Administration, Inhalation; D000485:Allergens / Q000276:immunology; D000818:Animals; D001249:Asthma / Q000276:immunology* / Q000473:pathology; D001980:Bronchi / Q000276:immunology; D016535:Bronchial Hyperreactivity / Q000276:immunology* / Q000473:pathology; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000276:immunology; D002908:Chronic Disease; D004195:Disease Models, Animal; D004802:Eosinophilia / Q000276:immunology; D004804:Eosinophils / Q000276:immunology; D016326:Extracellular Matrix Proteins / Q000276:immunology / Q000378:metabolism; D020397:Goblet Cells / Q000276:immunology; D007073:Immunoglobulin E / Q000097:blood; D007249:Inflammation / Q000276:immunology* / Q000473:pathology; D008168:Lung / Q000276:immunology / Q000473:pathology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D009130:Muscle, Smooth / Q000276:immunology; D010047:Ovalbumin / Q000276:immunology; D016212:Transforming Growth Factor beta / Q000032:analysis / Q000276:immunology
chemical_list: D000485:Allergens; D016326:Extracellular Matrix Proteins; D016212:Transforming Growth Factor beta; D007073:Immunoglobulin E; D010047:Ovalbumin