The study of pathophysiology, early intervention, and treatment for virus-induced asthma using a gene microarray analysis

由于病毒诱导的哮喘中嗜酸性粒细胞活化和细胞因子反应的信息很少，我们试图检测呼吸道病毒，并测量各种血清细胞因子/趋化因子，嗜酸性粒细胞阳离子蛋白（ECP）在急性和稳定性asthma.We检测病毒从急性哮喘患者的鼻灌洗液中获得抗原检测试剂盒或PCR，然后直接DNA测序分析。我们还检测了外周血嗜酸性粒细胞计数、血清ECP浓度和17种细胞因子/趋化因子（IL-1、3、2、4、5、6、7、8、10、12、13、17、IFN-γ、TNF-α、GM-CSF、G-CSF、MCP-1、和MIP-1β）在38例急性哮喘患者和51例未使用全身性皮质类固醇的稳定期哮喘患者中使用多重珠粒分析（Bio-Rad）。我们还利用基因芯片分析技术（Affytron）研究了哮喘患者刺激的嗜酸性粒细胞中高表达的基因。在157例急性哮喘患者中， ...更多信息 46例有病毒感染; 43例有RS病毒感染; 18例有肠道病毒感染; 18例有其他病毒感染; 32例无病毒感染。与哮喘稳定期相比，哮喘急性期ECP、IL-5、6、8和IL-10浓度显著升高，但嗜酸性粒细胞计数无显著变化。这些结果与鼻病毒诱导的哮喘和RS病毒诱导的哮喘中观察到的结果比稳定型哮喘中观察到的结果更相似。鼻病毒组仅IL-5水平显著高于RS病毒组。最后，我们发现一些基因，包括caspase 4，丝氨酸/苏氨酸激酶17 b，趋化因子（C-C基序）配体5，趋化因子（C-C基序）受体1在哮喘患者的人刺激嗜酸性粒细胞中上调。呼吸道病毒诱导的儿童哮喘的主要原因是鼻病毒和RS病毒。病毒诱导的哮喘，特别是鼻病毒诱导的哮喘，可能增强嗜酸性粒细胞的活化。此外，这些基因可能是哮喘嗜酸性粒细胞炎症的治疗靶点。少

Since little information is available on eosinophil activation and cytokine response in virus-induced asthma, we attempted to detect respiratory viruses and measure levels of various serum cytokines/chemokines, and eosinophil cationic protein (ECP) in acute as well as stable asthma.We detected viruses in nasal lavage obtained from patients with acute asthma using antigen detection kits or PCR followed by direct DNA sequencing analysis. We also measured peripheral eosinophil counts, concentrations of serum ECP, and 17 types of cytokines/chemokines (IL-1J3, 2, 4, 5, 6, 7, 8, 10, 12, 13, 17, IFN-γ, TNF-α, GM-CSF, G-CSF, MCP-1, and MIP-1β) using a multiplex beads-based assay (Bio-Rad) in 38 patients with acute asthma and in 51 patients with stable asthma who were not taking systemic corticosteroids. We also investigated the high expression gene in human stimulated eosinophils from patients with asthma using a gene microarray analysis (Affymetrix).Of the 157 acute asthma, rhinovirus was det … More ected in 46; RS virus, in 43; enterovirus, in 18; other viruses, in 18; and no viruses, in 32. The concentrations of ECP, IL-5, 6, 8, and IL-10, but not eosinophil counts, were significantly elevated in acute asthma as compared with those in stable asthma. These results were more similar to those observed in rhinovirus-induced asthma and RS virus-induced asthma than to those of stable asthma. Only the IL-5 level was significantly elevated in the rhinovirus group than in the RS virus. Finally, we found that several genes including caspase 4, serine/threonine kinase 17b, chemokine (C-C motif)ligand 5, chemokine (C-C motif) receptor 1 upregulated in human stimulated eosinophils obtained by asthmatic patients.The major causes of respiratory virus-induced childhood asthma were rhinovirus and RS virus.Virus-induced asthma, particularly those induced by rhinoviruses, might enhance eosinophil activation.Furthermore, these genes might be a therapeutic target for eosinophilic inflammation in asthma. Less