title: Development of respiratory syncytial virus "bronchiolitis" in guinea pigs does not reflect an allergic predisposition in the host.
abstract: BACKGROUND
  Respiratory syncytial virus (RSV) infection causes bronchiolitis in a minority of children. Using a guinea pig model to determine if an allergic predisposition in the host increases permissiveness to RSV infection or severity of experimental "bronchiolitis," we compared the effects of RSV inoculation between strain 2 (allergy-resistant) and strain 13 (allergy-susceptible) inbred animals.
  
  
  METHODS
  One month-old, juvenile guinea pigs were classified into four groups (eight guinea pigs per group): (group 1) strain 2, uninfected; (group 2) strain 13, uninfected; (group 3) strain 2, RSV infected; and (group 4) strain 13, RSV infected. Seven days after inoculation, the animals were studied by the following: viral plaque assays for quantification of intrapulmonary RSV; immunohistochemical localization of RSV antigens in lung tissue sections; physiologic assessment of airway obstruction and nonspecific bronchial hyperresponsiveness; quantitative histology of airway T lymphocytes, neutrophils, and eosinophils; and semiquantitative reverse transcriptase-polymerase chain reaction for levels of messenger RNA expression of a panel of proinflammatory cytokines and chemokines.
  
  
  RESULTS
  Significantly higher titers of replicating RSV were isolated from the lungs of strain 13 vs strain 2 animals (p < or = 0.001). The two guinea pig strains showed similar cell types with positive viral immunostaining; RSV-associated changes in airway obstruction and nonspecific bronchial hyperresponsiveness; airway T cells, neutrophils, and eosinophils; and messenger RNA expression of cytokines and chemokines.
  
  
  CONCLUSIONS
  Strain 13 guinea pigs show increased pulmonary RSV replication than strain 2 animals, but this increased permissiveness to the virus is not reflected by more severe virus-induced changes in airway obstruction, nonspecific bronchial hyperresponsiveness, airway inflammation, or gene expression of proinflammatory cytokines and chemokines.
authors.affiliation: UBC McDonald Research Laboratories and iCAPTURE Centre, Department of Pathology and Laboratory Medicine, St. Paul's Hospital, and The University of British Columbia, Vancouver, BC, Canada.
authors.forename: Andrew M
authors.initials: AM
authors.lastname: Bramley
authors.forename: M Aatif
authors.initials: MA
authors.lastname: Khan
authors.forename: Heather E
authors.initials: HE
authors.lastname: Manson
authors.forename: Richard G
authors.initials: RG
authors.lastname: Hegele
mesh_terms: D000485:Allergens; D000818:Animals; D000956:Antigens, Viral / Q000302:isolation & purification*; D001990:Bronchiolitis, Viral / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D004195:Disease Models, Animal; D006168:Guinea Pigs; D018357:Respiratory Syncytial Virus Infections / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D000485:Allergens; D000956:Antigens, Viral