title: Latent adenoviral infection modifies the steroid response in allergic lung inflammation.
abstract: BACKGROUND
  Steroid-resistant asthma develops after adenoviral bronchiolitis.
  
  
  OBJECTIVE
  We sought to determine the effect of steroids on allergic lung inflammation in the presence of latent adenoviral infection.
  
  
  METHODS
  Guinea pigs with latent adenoviral (n = 12) or sham (n = 12) infections were sensitized and challenged with ovalbumin (OA) or sham sensitized and challenged with saline solution. The effect of steroids (20 mg/kg administered intraperitoneally) on OA-induced lung inflammation was examined by using quantitative histology as the outcome measure.
  
  
  RESULTS
  Latent adenoviral infection increased CD8(+) cells in the airway wall and CD8(+) cells, macrophages, B cells, and CD4(+) cells in the lung parenchyma. Ovalbumin challenge, on the other hand, increased eosinophils, macrophages, B cells, and CD4(+) cells in both the airway wall and lung parenchyma independent of the effect of latent adenoviral infection. In the sham-infected groups steroid treatment caused the expected reduction in the eosinophilic infiltrate induced by OA challenge in the airways without affecting the other cells. In the presence of both latent adenoviral infection and OA challenge, steroid treatment had no effect on allergen-induced eosinophilia but reduced CD8(+) cells in the airways and CD8(+) cells, CD4(+) cells, and B cells in the parenchyma.
  
  
  CONCLUSIONS
  Latent adenoviral infection and OA challenge result in different types of lung inflammation, and the presence of latent adenoviral infection causes OA-induced eosinophilic airway inflammation to become steroid resistant.
authors.affiliation: University of British Columbia Pulmonary Research Laboratory, St Paul's Hospital, Vancouver, British Columbia, Canada.
authors.forename: K
authors.initials: K
authors.lastname: Yamada
authors.forename: W M
authors.initials: WM
authors.lastname: Elliott
authors.forename: S
authors.initials: S
authors.lastname: Hayashi
authors.forename: R
authors.initials: R
authors.lastname: Brattsand
authors.forename: C
authors.initials: C
authors.lastname: Roberts
authors.forename: T Z
authors.initials: TZ
authors.lastname: Vitalis
authors.forename: J C
authors.initials: JC
authors.lastname: Hogg
mesh_terms: D000257:Adenoviridae Infections / Q000276:immunology* / Q000378:metabolism / Q000473:pathology / Q000821:virology; D000260:Adenoviruses, Human / Q000276:immunology; D000287:Administration, Topical; D000485:Allergens / Q000008:administration & dosage / Q000009:adverse effects / Q000276:immunology; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D001249:Asthma / Q000188:drug therapy / Q000276:immunology* / Q000378:metabolism / Q000473:pathology / Q000821:virology; D001988:Bronchiolitis / Q000276:immunology* / Q000378:metabolism / Q000473:pathology / Q000821:virology; D019819:Budesonide / Q000627:therapeutic use*; D002460:Cell Line; D005260:Female; D005938:Glucocorticoids; D006168:Guinea Pigs; D006801:Humans; D008168:Lung / Q000276:immunology* / Q000378:metabolism / Q000473:pathology / Q000821:virology; D010047:Ovalbumin / Q000008:administration & dosage / Q000009:adverse effects / Q000276:immunology; D011014:Pneumonia / Q000276:immunology / Q000378:metabolism / Q000473:pathology / Q000821:virology; D017735:Virus Latency
chemical_list: D000485:Allergens; D000893:Anti-Inflammatory Agents; D005938:Glucocorticoids; D019819:Budesonide; D010047:Ovalbumin