title: Peripheral blood mononuclear cells from patients with bronchial asthma show impaired innate immune responses to rhinovirus in vitro.
abstract: BACKGROUND
  Asthmatic patients have a higher susceptibility to rhinovirus (RV) infection, and impaired IFN-β and IFN-λ production has been demonstrated in bronchial epithelial cells from asthmatic adults upon exposure to RV. However, the mechanisms underlying the increased susceptibility of asthmatic patients to RV infection remain poorly understood. The present study aimed to elucidate the characteristics of the immune responses of asthmatic patients' peripheral blood mononuclear cells (PBMCs) to RV exposure.
  
  
  METHODS
  PBMCs obtained from 3 different age groups (2-6 years: young-children group; 7-19 years: youth group; ≥20 years: adult group) of asthmatic patients and nonasthmatic control subjects were stimulated with RV-14 for 72 h. Healthy adults with a history of childhood asthma were also enrolled. The concentrations of IFN-α, IL-6, TNF-α, IL-10, and soluble Fas ligand (sFasL) in the culture supernatants were measured by ELISA.
  
  
  RESULTS
  When compared with age-matched control subjects, IFN-α production was significantly lower in the asthmatic youth group. IL-6, TNF-α, IL-10, and sFasL productions were significantly lower in both the asthmatic youth group and the adult group. Such impaired responses were not found in healthy adults with a history of childhood asthma. No significantly different responses were found between the asthmatics and controls in the young-children group, whereas young asthmatic children with persistent wheeze during a 2-year follow-up showed significantly lower IL-10 production than those without wheeze.
  
  
  CONCLUSIONS
  These results imply the involvement of impaired production of both IFN-α and inflammatory cytokines seen in asthmatic patients' PBMCs upon exposure to RV in the higher susceptibility of those patients to RV infection.
authors.affiliation: Department of Pediatrics, Jikei University School of Medicine, Tokyo, Japan.
authors.forename: Katsuhito
authors.initials: K
authors.lastname: Iikura
authors.forename: Toshio
authors.initials: T
authors.lastname: Katsunuma
authors.forename: Shizuko
authors.initials: S
authors.lastname: Saika
authors.forename: Saburo
authors.initials: S
authors.lastname: Saito
authors.forename: Sadato
authors.initials: S
authors.lastname: Ichinohe
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Ida
authors.forename: Hirohisa
authors.initials: H
authors.lastname: Saito
authors.forename: Kenji
authors.initials: K
authors.lastname: Matsumoto
mesh_terms: D000293:Adolescent; D000328:Adult; D000367:Age Factors; D001249:Asthma / Q000276:immunology* / Q000378:metabolism; D002478:Cells, Cultured; D002648:Child; D002675:Child, Preschool; D004198:Disease Susceptibility / Q000276:immunology; D053222:Fas Ligand Protein / Q000378:metabolism; D005260:Female; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology*; D016898:Interferon-alpha / Q000378:metabolism; D007371:Interferon-gamma / Q000378:metabolism; D016753:Interleukin-10 / Q000378:metabolism; D015847:Interleukin-4 / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000276:immunology* / Q000378:metabolism / Q000821:virology; D008297:Male; D010850:Picornaviridae Infections / Q000276:immunology; D012135:Respiratory Sounds / Q000276:immunology; D012229:Rhinovirus / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D055815:Young Adult
chemical_list: C505661:FASLG protein, human; D053222:Fas Ligand Protein; C508609:IL10 protein, human; C508598:IL4 protein, human; C508600:IL6 protein, human; D016898:Interferon-alpha; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D015847:Interleukin-4; D007371:Interferon-gamma