title: Effect of influenza A infection on umbilical cord blood natural killer function regulation with interleukin-15.
abstract: BACKGROUND
  Influenza A is a major pathogen of humans and has the potential to cause worldwide pandemics. Natural killer (NK) cells are important effector cells in the innate immune response against viruses, including influenza A. Infants are more susceptible to severe influenza A viral infection, possibly attributed in part to their defective NK function.
  
  
  METHODS
  We compared the NK responses to influenza using umbilical cord blood (UCB) and adult peripheral blood (APB) mononuclear cells and purified NK cells.
  
  
  RESULTS
  Influenza A induced dose-dependent apoptosis of NK cells with down-regulation of NKp46 expression, which was more pronounced in UCB. Both UCB and APB NK cells responded to influenza infection by up-regulating CD69 and CD107a expression, a process further enhanced by interleukin (IL) 15. Influenza exposure also down-regulated perforin expression and K562 cytotoxicity in UCB NK cells, which was partially restored by IL-15. The production of interferon (IFN) γ and tumor necrosis factor (TNF) α by NK cells in responding to influenza was further enhanced by IL-15.
  
  
  CONCLUSIONS
  Our findings show differential NK responses between newborns and adults. IL-15 may be beneficial in combating influenza by enhancing cytotoxic function and IFN-γ production.
authors.affiliation: Division of Asthma, Allergy, and Rheumatology, Chang Gung Memorial Hospital, Taoyuan, Taiwan.
authors.forename: Syh-Jae
authors.initials: SJ
authors.lastname: Lin
authors.forename: Po-Jen
authors.initials: PJ
authors.lastname: Cheng
authors.forename: Tzou-Yien
authors.initials: TY
authors.lastname: Lin
authors.forename: Pei-Tzu
authors.initials: PT
authors.lastname: Lee
authors.forename: Hsiu-Shan
authors.initials: HS
authors.lastname: Hsiao
authors.forename: Ming-Ling
authors.initials: ML
authors.lastname: Kuo
mesh_terms: D000328:Adult; D015703:Antigens, CD / Q000378:metabolism; D000945:Antigens, Differentiation, T-Lymphocyte / Q000378:metabolism; D017209:Apoptosis / Q000187:drug effects / Q000276:immunology; D003602:Cytotoxicity, Immunologic / Q000187:drug effects; D015536:Down-Regulation; D005312:Fetal Blood / Q000276:immunology*; D006801:Humans; D007231:Infant, Newborn; D009980:Influenza A virus / Q000276:immunology*; D007251:Influenza, Human / Q000276:immunology*; D007371:Interferon-gamma / Q000378:metabolism; D019409:Interleukin-15 / Q000276:immunology* / Q000494:pharmacology*; D020014:K562 Cells; D007694:Killer Cells, Natural / Q000166:cytology / Q000276:immunology*; D037181:Lectins, C-Type / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000276:immunology; D052118:Lysosomal-Associated Membrane Protein 1 / Q000378:metabolism; D055627:Natural Cytotoxicity Triggering Receptor 1 / Q000378:metabolism; D054353:Perforin / Q000378:metabolism; D018709:Statistics, Nonparametric; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D015854:Up-Regulation; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D007371:Interferon-gamma; D019409:Interleukin-15; D037181:Lectins, C-Type; D052118:Lysosomal-Associated Membrane Protein 1; D055627:Natural Cytotoxicity Triggering Receptor 1; D054353:Perforin; D014409:Tumor Necrosis Factor-alpha; D000099192:CD69 Antigens; C112260:NCR1 protein, human