title: Genistein attenuated allergic airway inflammation by modulating the transcription factors T-bet, GATA-3 and STAT-6 in a murine model of asthma.
abstract: BACKGROUND
  Genistein, a flavonoid in legumes and some herbal medicines, has various biological actions. Previous studies have shown that genistein decreased airway inflammation in allergic asthma. However, studies on how genistein affects immunoreactions in asthma are very limited.
  
  
  OBJECTIVE
  It was the aim of this study to investigate the effect of genistein on T helper 1 (Th1)/Th2 cytokines in a murine asthma model and to explore its underlying mechanisms.
  
  
  METHODS
  The asthma model was set up both in vivo and in vitro: the mice were divided into four groups in vivo, i.e. control group, ovalbumin-sensitized (OVA) group, Gen20 group (20 mg/kg genistein) and Gen40 group (40 mg/kg genistein), and into three groups in vitro, i.e. control group, OVA group, genistein group. Changes in lung histology were observed and concentrations of interleukin-4, interleukin-5 and interferon-γ in bronchoalveolar lavage fluid and serum were measured by enzyme-linked immunosorbent assay. The mRNA expression of GATA binding protein 3 (GATA-3), signal transducer and activator of transcription 6 (STAT-6) and T-box transcription factor (T-bet) in the lungs and CD4+ T cells of each group were detected by real-time PCR and the corresponding proteins were detected by Western blot.
  
  
  RESULTS
  The results showed that genistein attenuated OVA-induced airway inflammation, decreased Th2-type cytokines and increased Th1-type cytokines. Additionally, our data suggested that genistein may modulate the Th1/Th2 reaction by inhibiting GATA-3 and STAT-6 production while increasing T-bet production.
  
  
  CONCLUSIONS
  Genistein may modulate the immunomodulatory actions caused by Th1/Th2 cytokines in asthma, at least partially, by the down-regulation of GATA-3 and STAT-6 and the up-regulation of T-bet.
authors.affiliation: Emergency Department, Wuxi People's Hospital, Nanjing Medical University, Wuxi, PR China.
authors.forename: Fei
authors.initials: F
authors.lastname: Gao
authors.forename: Dong
authors.initials: D
authors.lastname: Wei
authors.forename: Tao
authors.initials: T
authors.lastname: Bian
authors.forename: Ping
authors.initials: P
authors.lastname: Xie
authors.forename: Jian
authors.initials: J
authors.lastname: Zou
authors.forename: Huijun
authors.initials: H
authors.lastname: Mu
authors.forename: Bin
authors.initials: B
authors.lastname: Zhang
authors.forename: Xiaoyan
authors.initials: X
authors.lastname: Zhou
mesh_terms: D000485:Allergens / Q000276:immunology; D000818:Animals; D018926:Anti-Allergic Agents / Q000627:therapeutic use*; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D001249:Asthma / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes / Q000187:drug effects / Q000276:immunology; D002478:Cells, Cultured; D016207:Cytokines / Q000097:blood / Q000276:immunology; D004195:Disease Models, Animal; D050990:GATA3 Transcription Factor / Q000235:genetics / Q000276:immunology; D019833:Genistein / Q000627:therapeutic use*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D010047:Ovalbumin / Q000276:immunology; D012333:RNA, Messenger / Q000276:immunology; D050800:STAT6 Transcription Factor / Q000235:genetics / Q000276:immunology; D020825:T-Box Domain Proteins / Q000235:genetics / Q000276:immunology; D000098815:T-bet Transcription Factor
chemical_list: D000485:Allergens; D018926:Anti-Allergic Agents; D000893:Anti-Inflammatory Agents; D016207:Cytokines; D050990:GATA3 Transcription Factor; C494748:Gata3 protein, mouse; D012333:RNA, Messenger; D050800:STAT6 Transcription Factor; C494100:Stat6 protein, mouse; D020825:T-Box Domain Proteins; D000098815:T-bet Transcription Factor; D010047:Ovalbumin; D019833:Genistein