RESUMEN
Objective To investigate the impact of eotaxin-3 gene polymorphisms on the clinical effect of inhaled corticosteroids (ICS) to provide clinical basis for eotaxin-3 as the target spot for treating bronchial asthma.Methods One hundred and ninety-six cases of asthma and 196 cases as controls were selected from the outpatients and inpatients in our hospital.Peripheral blood samples were collected from the asthma patients and normal controls.PCR-RFLP was adopted to detect the genotypes of eotaxin-3 +2497T＞G and-+-77C＞T.The response of ICS treatment and the change situation of ACT scores were compared among asthmatic patients with various genotypes.Results Peripheral blood eosinophil(EOS) counts,EOS proportion and total IgE in the patients with TG genotype at+2497 locus were significantly decreased compared with those in the patients with TT genotype,the difference was statistically significant(P＜0.05).The level of PD20 in asthmatic patients with TG genotype was significantly higher than that in the patients with TT genotype,the difference was statistically significant[(0.07-±-0.03)mg vs.(0.03 ± 0.01)mg,t=2.45,P=0.048];whereas the above indicators had no statistical difference among 3 kinds of +-77 genotypes.During ICS treatment process in the patients with TT genotype at +-2497 locus,the FEV1％,PD20 value and ACT scores were significantly improved compared with those in the patients with TG genotype,the difference was statistically significant(P＜0.01).Conclusion The asthmatic patients with TT genotype at +-2497 locus were more sensitive to ICS treatment,regular ICS treatment can significantly improve the lung function and clinical symptom score in these patients.
RESUMEN
Objective To investigate the impact of eotaxin-3 gene polymorphisms on the clinical effect of inhaled corticosteroids (ICS) to provide clinical basis for eotaxin-3 as the target spot for treating bronchial asthma.Methods One hundred and ninety-six cases of asthma and 196 cases as controls were selected from the outpatients and inpatients in our hospital.Peripheral blood samples were collected from the asthma patients and normal controls.PCR-RFLP was adopted to detect the genotypes of eotaxin-3 +2497T＞G and-+-77C＞T.The response of ICS treatment and the change situation of ACT scores were compared among asthmatic patients with various genotypes.Results Peripheral blood eosinophil(EOS) counts,EOS proportion and total IgE in the patients with TG genotype at+2497 locus were significantly decreased compared with those in the patients with TT genotype,the difference was statistically significant(P＜0.05).The level of PD20 in asthmatic patients with TG genotype was significantly higher than that in the patients with TT genotype,the difference was statistically significant[(0.07-±-0.03)mg vs.(0.03 ± 0.01)mg,t=2.45,P=0.048];whereas the above indicators had no statistical difference among 3 kinds of +-77 genotypes.During ICS treatment process in the patients with TT genotype at +-2497 locus,the FEV1％,PD20 value and ACT scores were significantly improved compared with those in the patients with TG genotype,the difference was statistically significant(P＜0.01).Conclusion The asthmatic patients with TT genotype at +-2497 locus were more sensitive to ICS treatment,regular ICS treatment can significantly improve the lung function and clinical symptom score in these patients.
RESUMEN
Objective To investigate whether leukotriene D4 (LTD4) regulates eotaxin-3 (Eot-3) expression in bronchial epithelial cells, and study effect of pranlukst on the regulation.Methods BEAS-2B cells and normal human bronchial epithelia cells were pre- treated with LTD4 for 1 hour,stimulated with interleukin-4, the cells were incubated for 24 hours. Eot-3 protein in supernatant were measured by enzyme linked immunosorbent assay(ELISA). The cells were pretreated with pranlukast in different concentration, then the above procedure was repeated. Results The untreated bronchial epithelial cell expressed Eot-3 protein on a very low level. After stimulating with IL-4 and incubating for 24 hours, Eot-3 production increased significantly. Pretreating the cells with LTD4 enhanced the inducing effect of IL-4. Pranlukast inverted the upregulation of LTD4. Conclusions Upregulating the expression of Eot-3 induced by IL-4 on bronchial epithelial cells may explain partially the mechanism of leukotrienes involving airway allergic inflammation of asthma. The invertion impact on upregulation of LTD4 by pranlukast may be one of mechanisms that leukotrienes receptor antagonist cure asthma.