title: Analysis of gene expressions of T cells from children with acute exacerbations of asthma.
abstract: BACKGROUND
  Little is known about airway inflammation in childhood asthma. The aims of this study were to analyze the expression of a wide range of mediators of airway inflammation in childhood asthma.
  
  
  METHODS
  Eight asthmatic children with acute exacerbations were recruited for the study. Peripheral blood was drawn from the patients at the time of exacerbation and after improvement. Total RNA was extracted from the isolated T lymphocytes. The differential display (DD) RT-PCR method was used to detect expressed genes, and the quantification of candidate gene expression was performed using real-time quantitative RT-PCR.
  
  
  RESULTS
  The only gene for which significant expression differences were detected in both DD analysis and quantitative RT-PCR was lipocortin II (annexin II) (exacerbation > remission, p < 0.05). In quantitative RT-PCR of interleukin-4 (IL-4), IL-5, interferon-gamma, IL-12 receptor-beta and integrin alpha6, a significant difference was found only in the expression of IL-4 mRNA (exacerbation > remission, p < 0.05). The IL-4 plasma concentration tended to be higher in exacerbation than in remission.
  
  
  CONCLUSIONS
  Our findings suggest activation of T cells and IL-4 production may be involved not only in the basic pathogenesis of childhood asthma but also in its acute exacerbation, and that lipocortin II may be a marker or contribute to asthma exacerbation.
authors.affiliation: Department of Pediatrics, Jikei University School of Medicine, Tokyo, Japan. tkatsunuma@jikei.ac.jp
authors.forename: Toshio
authors.initials: T
authors.lastname: Katsunuma
authors.forename: Hidetoshi
authors.initials: H
authors.lastname: Kawahara
authors.forename: Tomoko
authors.initials: T
authors.lastname: Suda
authors.forename: Tetsuji
authors.initials: T
authors.lastname: Ishii
authors.forename: Yukihiro
authors.initials: Y
authors.lastname: Ohya
authors.forename: Akira
authors.initials: A
authors.lastname: Akasawa
authors.forename: Hirohisa
authors.initials: H
authors.lastname: Saito
authors.forename: Tadahiro
authors.initials: T
authors.lastname: Oshida
authors.forename: Yuji
authors.initials: Y
authors.lastname: Sugita
mesh_terms: D000208:Acute Disease; D017306:Annexin A2 / Q000096:biosynthesis / Q000235:genetics; D001249:Asthma / Q000235:genetics*; D002648:Child; D002669:Child Welfare; D005260:Female; D015870:Gene Expression / Q000235:genetics*; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation; D020022:Genetic Predisposition to Disease / Q000235:genetics; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D039503:Integrin alpha6 / Q000096:biosynthesis / Q000235:genetics; D007371:Interferon-gamma / Q000096:biosynthesis / Q000235:genetics; D015847:Interleukin-4 / Q000096:biosynthesis / Q000235:genetics; D015848:Interleukin-5 / Q000096:biosynthesis / Q000235:genetics; D008297:Male; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D018123:Receptors, Interleukin / Q000096:biosynthesis / Q000235:genetics; D053707:Receptors, Interleukin-12; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013601:T-Lymphocytes / Q000502:physiology*
chemical_list: D017306:Annexin A2; D018836:Inflammation Mediators; D039503:Integrin alpha6; D015848:Interleukin-5; D012333:RNA, Messenger; D018123:Receptors, Interleukin; D053707:Receptors, Interleukin-12; D015847:Interleukin-4; D007371:Interferon-gamma