Return to Contents in this Issue

Original Article


Severity of Asthma: The Role of CD25+,CD30+, NF-κB, and Apoptotic Markers


AS Abdulamir,1,4 HS Kadhim,1,4 RR Hafidh,2 MA Ali,1 I Faik,1 F Abubakar,2 KA Abbas3

1 Microbiology Research Department, University Putra Malaysia, Serdang, Malaysia
2 Institute of Bioscience, University Putra Malaysia, Serdang, Selangor Darul Ehsan, Malaysia
3 Faculty of Food Science and Technology, University Putra Malaysia, Serdang, Malaysia
4 Microbiology Department, Faculty of Medicine, Al-Nahrain University, Baghdad, Iraq

J Investig Allergol Clin Immunol 2009; Vol. 19(3): 218-224



Objectives: 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-κB 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-κB, 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-κB, Bcl-2, and Bcl-2/Bax increased, whereas those of Bax decreased, progressively, from MA to SA (P<.05). NF-κB 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 infl ammatory 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-κB 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-κB, which in turn blocks the proapoptotic potential of CD30 induction itself.

Key words: Asthma. Apoptosis. Memory cells. CD45RO. TH1. TH2. IL-4. IFN-γ.