title: Severity of asthma: the role of CD25+, CD30+, NF-kappaB, and apoptotic markers.
abstract: OBJECTIVE
  We studied the role of the regulatory T cells CD4+CD25+ (Treg) and activated CD4+CD30+ cells in the pathogenesis of asthma and their association with apoptosis and NF-kappaB in patients with mild intermittent asthma (MA), severe persistent asthma (SA), and healthy volunteers (HV).
  
  
  METHODS
  Peripheral blood lymphocytes (PBL) were extracted from asthmatic patients during exacerbations, and CD4+ cells were separated using Dynal beads. Immunostaining of whole PBL for NF-kappaB, Bax, and Bcl-2, and immunostaining of CD4+ cells for CD25+ and CD30+ cells were performed using immunocytochemistry.
  
  
  RESULTS
  Treg cells were expressed at higher levels in MA than in HV and SA (P < .05), while CD30+ T cells were expressed at higher levels in both SA and MA than in HV (P < .05), although there was no remarkable difference between SA and MA (P>.05). Levels of NF-kappaB, Bcl-2, and Bcl-2/Bax increased, whereas those of Bax decreased, progressively, from MA to SA (P < .05). NF-kappaB levels correlated directly with the Bcl-2/Bax ratio and with CD4+CD30+ cells in SA and MA, whereas CD4+CD30+ cells correlated inversely with the Bcl-2/Bax ratio.
  
  
  CONCLUSIONS
  Unregulated Treg cells probably return inflammatory responses to normal values during exacerbations in MA; however, expression of Treg cells was extensively diminished in SA, leading to probable loss of suppressive control over underlying immune reactions. CD4+CD30+ cells were associated with the pathogenesis of asthma but not with severity. NF-kappaB seems to be the central inflammatory factor in SA, with a remarkable loss of PBL apoptosis, diminished Treg levels, and high CD30+ cell levels that probably induce NF-kappaB, which in turn blocks the proapoptotic potential of CD30 induction itself.
authors.affiliation: Microbiology Research Department, University Putra Malaysia, Serdang, Malaysia. ahmsah73@yahoo.com
authors.forename: A S
authors.initials: AS
authors.lastname: Abdulamir
authors.forename: H S
authors.initials: HS
authors.lastname: Kadhim
authors.forename: R R
authors.initials: RR
authors.lastname: Hafidh
authors.forename: M A
authors.initials: MA
authors.lastname: Ali
authors.forename: I
authors.initials: I
authors.lastname: Faik
authors.forename: F
authors.initials: F
authors.lastname: Abubakar
authors.forename: K A
authors.initials: KA
authors.lastname: Abbas
mesh_terms: D000293:Adolescent; D000328:Adult; D017209:Apoptosis / Q000276:immunology*; D001249:Asthma / Q000175:diagnosis* / Q000276:immunology* / Q000378:metabolism; D015415:Biomarkers / Q000032:analysis; D015704:CD4 Antigens / Q000276:immunology; D005260:Female; D006801:Humans; D053645:Interleukin-2 Receptor alpha Subunit / Q000276:immunology; D017730:Ki-1 Antigen / Q000276:immunology / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D016328:NF-kappa B / Q000276:immunology / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000276:immunology / Q000378:metabolism; D050378:T-Lymphocytes, Regulatory / Q000276:immunology* / Q000378:metabolism; D055815:Young Adult; D051028:bcl-2-Associated X Protein / Q000276:immunology / Q000378:metabolism
chemical_list: D015415:Biomarkers; D015704:CD4 Antigens; D053645:Interleukin-2 Receptor alpha Subunit; D017730:Ki-1 Antigen; D016328:NF-kappa B; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein