title: Dendritic cells modulated by cytokine-expressing adenoviruses alleviate eosinophilia and airway hyperresponsiveness in an animal model of asthma.
abstract: BACKGROUND
  It has been found that TH1-related cytokines can decrease the accumulation of eosinophils in lung tissue and relieve airway constriction.
  
  
  OBJECTIVE
  Dendritic cells (DCs) have been found to prime naive T-helper cells efficiently. In this study, DCs infected with TH1 cytokine-expressing adenovirus can be used to induce antigen-specific TH1 cells for treatment in an animal model of asthma.
  
  
  METHODS
  Cytokine gene-modulated DCs pulsed with ovalbumin antigen (OVA) were injected intravenously into naive mice 1 week before sensitization with OVA antigen. The mice were then monitored for OVA-specific IgE, airway inflammatory cell infiltration, and airway hyperresponsiveness in the study.
  
  
  RESULTS
  Significant levels of IL-12 or IL-18 were expressed by Ad-IL-12 or Ad-IL-18 infected, bone marrow-derived DCs. Ad-IL-12 and Ad-IL-18 co-infected DCs effectively, decreasing sera anti-OVA IgE antibody levels, lung eosinophilia, and airway hyperresponsiveness.
  
  
  CONCLUSIONS
  We concluded that DCs modulated by TH1-prone cytokine-expressing adenoviruses can alleviate TH2-type airway inflammation in a murine model and can provide possible therapeutic application for DCs in asthma.
authors.affiliation: Department of Medical Technology, Chung Hwa College of Medical Technology, Tainan, Taiwan, Republic of China.
authors.forename: Yi-Ling
authors.initials: YL
authors.lastname: Ye
authors.forename: Yueh-Lun
authors.initials: YL
authors.lastname: Lee
authors.forename: Zen-Jai
authors.initials: ZJ
authors.lastname: Chuang
authors.forename: Huai-Jean
authors.initials: HJ
authors.lastname: Lai
authors.forename: Chun-Chi
authors.initials: CC
authors.lastname: Chen
authors.forename: Mi-Hua
authors.initials: MH
authors.lastname: Tao
authors.forename: Bor-Luen
authors.initials: BL
authors.lastname: Chiang
mesh_terms: D000256:Adenoviridae / Q000276:immunology*; D000818:Animals; D001249:Asthma / Q000150:complications / Q000276:immunology*; D016535:Bronchial Hyperreactivity / Q000150:complications / Q000276:immunology*; D016207:Cytokines / Q000276:immunology; D003713:Dendritic Cells / Q000276:immunology*; D004802:Eosinophilia / Q000150:complications / Q000276:immunology*; D018664:Interleukin-12 / Q000276:immunology; D020382:Interleukin-18 / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D023421:Models, Animal; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
chemical_list: D016207:Cytokines; D020382:Interleukin-18; D018664:Interleukin-12