摘要
Objective To investigate the cytokines responsible for pathophysiology of asthma. Methods In vitro effects of recombinant interleukin 4 (rIL 4) and interferon gamma (IFN γ) on synthesis of immunoglobulin E (IgE) by peripheral blood mononuclear cells (PBMC) were studied in 30 asthmatic patients and 25 normal controls. Results Spontaneous IgE synthesis by PBMC significantly increased in patients with asthma compared with the controls (t=4.471, P<0.001). Although the maximun amounts of IgE synthesis using PBMC after stimulation with rIL 4 were almost the same in the patients with asthma and in the controls (P>0.05), the enhancement rate of rIL 4 induced IgE synthesis was lower in the asthma patients than in the controls (t= 4.6719, P<0.005). IFN γ suppressed both spontaneous and rIL 4 induced IgE synthesis by PBMC in the asthma patients. The suppressive effect on IgE synthesis was more prominent in the patients with asthma than in the controls (t=7.1833, P< 0.001). Conclusions Asthma attacks are related to IgE dependant trigger mechanism. The imbalance of IL 4 and IFN γ in vivo is the cause of elevated IgE that can produce mediators release and asthma attacks. IFN γ can inhibit IgE synthesis, so IFN γ may be a new approach to the treatment of asthma.
Objective To investigate the cytokines responsible for pathophysiology of asthma. Methods In vitro effects of recombinant interleukin 4 (rIL 4) and interferon gamma (IFN γ) on synthesis of immunoglobulin E (IgE) by peripheral blood mononuclear cells (PBMC) were studied in 30 asthmatic patients and 25 normal controls. Results Spontaneous IgE synthesis by PBMC significantly increased in patients with asthma compared with the controls (t=4.471, P<0.001). Although the maximun amounts of IgE synthesis using PBMC after stimulation with rIL 4 were almost the same in the patients with asthma and in the controls (P>0.05), the enhancement rate of rIL 4 induced IgE synthesis was lower in the asthma patients than in the controls (t= 4.6719, P<0.005). IFN γ suppressed both spontaneous and rIL 4 induced IgE synthesis by PBMC in the asthma patients. The suppressive effect on IgE synthesis was more prominent in the patients with asthma than in the controls (t=7.1833, P< 0.001). Conclusions Asthma attacks are related to IgE dependant trigger mechanism. The imbalance of IL 4 and IFN γ in vivo is the cause of elevated IgE that can produce mediators release and asthma attacks. IFN γ can inhibit IgE synthesis, so IFN γ may be a new approach to the treatment of asthma.
