title: Cytokine production from peripheral blood mononuclear cells of mite allergen-sensitized atopic adults stimulated with respiratory syncytial virus and mite allergen.
abstract: BACKGROUND
  The interaction between viral respiratory tract infection and allergen sensitization in allergic asthma is unclear. Respiratory syncytial virus (RSV) has attracted attention as an important lower respiratory pathogen during childhood, while recent evidence indicates that RSV is also an important lower respiratory pathogen for adults. Immunity against RSV differs between children and adults. Several reports suggest that RSV infection in children results in a Th2-skewed immune response. The purpose of the present study was to determine the effects of RSV infection in adults who had previously been sensitized with a common aeroallergen.
  
  
  METHODS
  Peripheral blood mononuclear cells (PBMCs) isolated from 9 mite-sensitized atopic subjects and 11 healthy nonatopic subjects were exposed to live or UV-inactivated RSV concomitant to incubation with or without mite allergen, and the subsequent production of cytokines - interleukin (IL)-5, interferon (IFN)-gamma, IL-10 and IL-12p70 - was measured.
  
  
  RESULTS
  Mite allergen significantly increased IL-5 production in atopic PBMCs. RSV infection significantly increased IFN-gamma production from healthy and atopic PBMCs; the levels of IFN-gamma were significantly higher for atopic PBMCs. Live RSV infection significantly attenuated IL-5 production from mite allergen-stimulated atopic PBMCs. UV-inactivated RSV, but not live RSV, significantly enhanced allergen-specific IL-10 production in atopic PBMCs. IL-12 could not be detected in the present study.
  
  
  CONCLUSIONS
  The present findings suggest that RSV infection did not simply enhance allergen-specific Th2-like response in atopic adults. Live RSV-induced IFN-gamma and RSV protein-induced IL-10 appear to play important roles in the regulation of allergic airway inflammation in atopic adults.
authors.affiliation: Second Department of Internal Medicine, Nagasaki University School of Medicine, Nagasaki, Japan.
authors.forename: Hiroko
authors.initials: H
authors.lastname: Hirose
authors.forename: Hiroto
authors.initials: H
authors.lastname: Matsuse
authors.forename: Tomoko
authors.initials: T
authors.lastname: Tsuchida
authors.forename: Susumu
authors.initials: S
authors.lastname: Fukahori
authors.forename: Chizu
authors.initials: C
authors.lastname: Fukushima
authors.forename: Yohei
authors.initials: Y
authors.lastname: Mizuta
authors.forename: Shigeru
authors.initials: S
authors.lastname: Kohno
mesh_terms: D000328:Adult; D000485:Allergens / Q000276:immunology*; D000818:Animals; D045744:Cell Line, Tumor; D002478:Cells, Cultured; D002648:Child; D016207:Cytokines / Q000096:biosynthesis*; D040001:Dermatophagoides farinae / Q000276:immunology*; D005260:Female; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000276:immunology* / Q000821:virology; D007963:Leukocytes, Mononuclear / Q000276:immunology* / Q000378:metabolism / Q000821:virology; D008297:Male; D012136:Respiratory Syncytial Viruses / Q000276:immunology* / Q000472:pathogenicity; D018418:Th2 Cells / Q000276:immunology / Q000378:metabolism / Q000821:virology; D015854:Up-Regulation / Q000276:immunology
chemical_list: D000485:Allergens; D016207:Cytokines