Dong-xia Yang1, Na Li, Xiao-lin Zhang, Qi Wang. 1. Department of Respiratory Disease, the Second Affiliated Hospital of Dalian Medical University, Dalian 116000, China.
Abstract
OBJECTIVE: To study the levels of serum interleukin (IL)-18 and IL-33 in asthmatic patients pre-and post-treatment with glucocorticoids during the acute exacerbation period and therefore to investigate the role of IL-18 and IL-33 in the pathogenesis of bronchial asthma. METHODS: Thirty cases of moderate to severe asthma admitted in the Second Affiliated Hospital of Dalian Medical University from June, 2009 to October, 2010 were chosen as the asthma group, and 23 healthy people who underwent routine physical examination were chosen as the control group. The subjects in the 2 groups were all nonsmokers. All the patients were treated with a glucocorticoid (methylprednisolone 40 - 80 mg/d) for 3 to 5 days and combined with aerosol inhalation of budesonide for 1 to 2 weeks as adjuvant therapy. The serum levels of IL-18 and IL-33 were detected for the asthma group before and after the treatment and for the control group. Other data including immunoglobulin E (IgE), the number of eosinophil cells (EOS) and the pulmonary function (FEV(1)%pre) were measured as well. The differences of IL-18 and IL-33 levels between the asthma group before and after treatment and the control group were analyzed, and the correlation between IL-18, IL-33 and IgE, EOS and FEV(1)%pre were analyzed as well by SPSS software. RESULTS: Compared with the healthy control group [(158 ± 45) ng/L and (143 ± 32) ng/L], the levels of IL-18 and IL-33 in the asthma pre-treatment group were significantly increased [(300 ± 181) ng/L and (208 ± 95) ng/L, t = 3.67 and 3.51, all P < 0.05)]; and the IgE level and EOS count showed a similar change (t = 5.76 and 5.24, all P < 0.05). After systemic glucocorticoid treatment and local aerosol inhalation, the levels of IL-18 and IL-33 [(183 ± 83) ng/L and (148 ± 77) ng/L] were decreased significantly in the asthma patients [t = 5.42 and 12.09, all P < 0.05], and the IgE level and EOS count also showed a same trend as well (t = 11.87 and 4.56, all P < 0.05), whereas FEV(1)%pred [(54 ± 14)%] increased significantly [(81 ± 16)%, t = -7.81, P < 0.05]. The Pearson correlative analysis showed that there were positive correlations between the levels of IL-18, IL-33 and IgE and EOS, respectively (all P < 0.05), and there were negative correlations between IL-18, IL-33 levels and FEV(1)%pre, respectively (all P < 0.05). CONCLUSIONS: Our results suggest that IL-18 and IL-33 participate in the pathogenesis of asthma, and may play stimulation role in the process of the disease.
OBJECTIVE: To study the levels of serum interleukin (IL)-18 and IL-33 in asthmatic patients pre-and post-treatment with glucocorticoids during the acute exacerbation period and therefore to investigate the role of IL-18 and IL-33 in the pathogenesis of bronchial asthma. METHODS: Thirty cases of moderate to severe asthma admitted in the Second Affiliated Hospital of Dalian Medical University from June, 2009 to October, 2010 were chosen as the asthma group, and 23 healthy people who underwent routine physical examination were chosen as the control group. The subjects in the 2 groups were all nonsmokers. All the patients were treated with a glucocorticoid (methylprednisolone 40 - 80 mg/d) for 3 to 5 days and combined with aerosol inhalation of budesonide for 1 to 2 weeks as adjuvant therapy. The serum levels of IL-18 and IL-33 were detected for the asthma group before and after the treatment and for the control group. Other data including immunoglobulin E (IgE), the number of eosinophil cells (EOS) and the pulmonary function (FEV(1)%pre) were measured as well. The differences of IL-18 and IL-33 levels between the asthma group before and after treatment and the control group were analyzed, and the correlation between IL-18, IL-33 and IgE, EOS and FEV(1)%pre were analyzed as well by SPSS software. RESULTS: Compared with the healthy control group [(158 ± 45) ng/L and (143 ± 32) ng/L], the levels of IL-18 and IL-33 in the asthma pre-treatment group were significantly increased [(300 ± 181) ng/L and (208 ± 95) ng/L, t = 3.67 and 3.51, all P < 0.05)]; and the IgE level and EOS count showed a similar change (t = 5.76 and 5.24, all P < 0.05). After systemic glucocorticoid treatment and local aerosol inhalation, the levels of IL-18 and IL-33 [(183 ± 83) ng/L and (148 ± 77) ng/L] were decreased significantly in the asthma patients [t = 5.42 and 12.09, all P < 0.05], and the IgE level and EOS count also showed a same trend as well (t = 11.87 and 4.56, all P < 0.05), whereas FEV(1)%pred [(54 ± 14)%] increased significantly [(81 ± 16)%, t = -7.81, P < 0.05]. The Pearson correlative analysis showed that there were positive correlations between the levels of IL-18, IL-33 and IgE and EOS, respectively (all P < 0.05), and there were negative correlations between IL-18, IL-33 levels and FEV(1)%pre, respectively (all P < 0.05). CONCLUSIONS: Our results suggest that IL-18 and IL-33 participate in the pathogenesis of asthma, and may play stimulation role in the process of the disease.