染色体1q12 区段IL6R 基因多态性与儿童哮喘易感性的研究

目的:检测染色体1q12区段IL6R基因多态性与儿童发生支气管哮喘易感性的关系。方法:150名支气管哮喘患儿为支气管哮喘组。150名健康儿童为对照组。采用质谱单核苷酸多态性(SNP)技术,对两组儿童的IL6R基因进行分析。结果:两组IL6基因位点的分布符合Hardy-Weinburg平衡定律。两组IL6R基因rs4845374位点的基因型与等位基因相比较,无明显差异(X2值分别为3.442和3.701;P值分别为0.179和0.088)。两组IL6R基因rs2228145位点的基因型与等位基因相比较,差异均有统计学意义(X2值分别为6.635和9.200;P值分别为0.036和0.003)。IL6R基因rs2228145位点基因型的变异等位基因T、C与支气管哮喘存在密切联系,CC、TT型出现支气管哮喘的风险均比CT型高。结论:IL6R基因rs4845374位点与儿童支气管哮喘无相关性,而rs2228145位点多态性与儿童支气管哮喘有相关性。     

布地奈德联合孟鲁司特钠对支气管哮喘患儿细胞因子、免疫功能影响

目的:探讨布地奈德联合孟鲁司特钠对支气管哮喘患儿细胞因子、免疫功能影响。方法:选自我院于2014年9月~2016年3月期间收治的支气管哮喘患儿96例,依据随机数字表法随机分为观察组与对照组,每组48例。对照组给予孟鲁司特钠治疗,观察组在对照组基础上结合布地奈德治疗。两组疗程均为4周。观察并比较两组的临床疗效、以及治疗前后患者血清细胞因子水平、免疫功能及肺功能的变化情况。结果:观察组治疗总有效率(95.83%)高于对照组(79.17%)(P0.05);观察组血清IL-5含量治疗后低于对照组,而IL-12含量高于对照组(P0.05);观察组血清Ig E含量治疗后低于对照组,而Ig A、Ig M含量高于对照组(P0.05);观察组FEV1和FVC治疗后高于对照组(P0.05);两组均未见明显不良反应。结论:布地奈德联合孟鲁司特钠治疗支气管哮喘患儿疗效显著,且作用可能与改善细胞因子、免疫功能及肺功能有关。     

支气管哮喘患儿病情控制的影响因素及其家长知信行问卷调查分析

摘要 目的：调查支气管哮喘患儿家长知信行情况,并分析支气管哮喘患儿病情控制的影响因素。方法：于2016年7月~2020年7月期间,选取我院收治的500例支气管哮喘患儿及其家长作为研究对象。患儿家长知信行情况采用《哮喘患儿家长知信行问卷》调查。患儿近4周的病情控制水平参照《诸福棠实用儿科学(第8版)》中的相关标准进行确定,病情控制水平包括良好控制、部分控制和未控制。将良好控制、部分控制的患儿纳为哮喘控制组,将未控制的患儿纳为哮喘未控制组。采用本院自制的调查量表调查患儿及其家长的信息,分析支气管哮喘患儿病情控制的影响因素。结果：支气管哮喘儿童家长知信行情况不容乐观。支气管哮喘患儿病情控制率为38.06%（187/491）。单因素分析结果表明,支气管哮喘患儿病情控制与家庭人均月收入、患儿个人过敏史、家长受教育程度、哮喘家族史、是否坚持长期用药、是否定期复诊有关（P<0.05）。多因素Logistic回归分析结果显示,家长受教育程度、家庭人均月收入、患儿个人过敏史、哮喘家族史、是否坚持长期用药、是否定期复诊均是支气管哮喘患儿病情控制的影响因素（P<0.05）。结论：本研究中支气管哮喘患儿病情控制水平一般,且支气管哮喘儿童家长知信行情况不容乐观,其中家长受教育程度、家庭人均月收入、患儿个人过敏史等均是支气管哮喘患儿病情控制的影响因素,临床中应结合相关因素进行针对性的干预或治疗,以期实现对支气管哮喘患儿病情的良好控制。     

Influence of <Emphasis Type="Italic">TRPV4</Emphasis> gene polymorphisms on the development of osmotic airway hyperresponsiveness in patients with bronchial asthma

The effect of single nucleotide polymorphisms (SNP) of TRPV4 gene on the development of airway hyperresponsiveness (39.7% of cases) in response to the decrease in osmolarity under inspiration of distilled water aerosol was studies in 189 patients with uncontrolled bronchial asthma. rs6606743 SNP was found to significantly contribute to the development of osmotic airway hyperresponsiveness. Analysis of the dominant genetic model revealed substantial prevalence of AG + GG genotype frequency in the group of patients with asthma with osmotic hyperresponsiveness in comparison with the patients who had negative response to bronchoprovocation. In addition, carriers of GG or AG genotypes had significantly more profound decrease of lung function parameters in relation to A homozygous patients.     

Correlation Between IL-13rs20541(A> G) Gene Polymorphism and Bronchial Asthma Among Iraqi Patients

Background:Bronchial asthma has a complicated genetic history. Changes in gene expression may be caused by gene polymorphism, cytokines play a central role. IL-13 is an interleukin that has been shown to play a role in the disease''s immunopathogenesis. The current study investigated the relationship between rs20541 of the IL-13 gene and Bronchial asthma in Iraqi patients.Methods:Seventy-five patient and fifty healthy individuals as a control. The DNA was extracted from blood samples. Detection of genotype IL-13SNP (rs20541) were achieved by RFLP-PCR.Results:indicated a highly significant the levels of the IgE, and IL-13 in the patients compared to control at (p value≤ 0.01), (456.45±290.106 vs. 30.08±24.414), (59.5980±20.93750 vs.6.7034±4.10547) pg/ml respectively. Result shows no significant differences in the frequency distributions of IL-13 SNP (rs20541) for all genotypes in cases and controls. A protective role of asthma, (OR: 0.62; CI.95%: 0.23 - 1.6) and (OR 0.89; CI.95%:0.42 - 1.89) were observed for wild type homozygous and heterozygous genotype respectively. Whereas the AA genotype (42.7%) in cases and (34.0%) in control, that (OR:1.44; CI.95%:( 0.66 - 3.07) mutant homozygous were risk factors of asthma among individuals. The genotypes of IL-13 rs20541 (GG, AG, AA) among patients and controls were significantly correlated with IgE and IL-13 results at (p≤ 0.05).Conclusion:AA genotype in case and control mutant homozygous were risk factors of asthma among individuals. It’s possible that this has a predisposing impact on the development of asthma.Key Words: Bronchial Asthma, RFLP, IL-13, SNP     

Retracted: The role of HOTAIR-induced downregulation of microRNA-126 and interleukin-13 in the development of bronchial hyperresponsiveness in neonates

Long noncoding RNAs, including HOTAIR, are involved in the pathogenesis of a wide range of diseases. This study aimed to explore the mechanism underlying the involvement of HOTAIR in neonatal bronchial hyperresponsiveness (BHR). A total of 105 newborns were recruited in this study to collect their peripheral blood mononuclear cell and serum samples, which were then divided into different genotype groups based on the genotypes of rs4759314, rs874945, and rs7958904. The real-time polymerase chain reaction, western blot analysis, computational analyses, and luciferase assays were performed to establish the regulatory relationships between the HOTAIR, microRNA-126 (miR-126), and interleukin-13 (IL-13). The level of HOTAIR, miR-126, and IL-13 among rs4759314 AA, AG, and GG groups, as well as among rs874945 GG, AG, and AA groups was similar. However, the level of HOTAIR was increased in the rs7958904 GG group, accompanied by a decreased level of miR-126 and IL-13. In addition, the level of airway responsiveness was comparable among rs4759314 AA, AG, and GG groups, as well as among rs874945 GG, AG, and AA groups. However, the airway responsiveness in the groups rs7958904 CG and CC was much stronger than that of the GG group. We also demonstrated that, by directly binding to miR-126, HOTAIR reduced the expression of miR-126, which in turn decreased the expression of IL-13. In summary, we demonstrated the role of HOTAIR-induced downregulation of miR-126 and IL-13 in the development of BHR in neonates.     

肠道菌群失调和免疫失衡与儿童支气管哮喘的关系

研究儿童支气管哮喘与肠道菌群失调和免疫失衡的关系。

选择2019年1月至2021年1月我院儿科门诊收治的46例哮喘患儿为哮喘组,并以同期32例健康儿童为对照组。哮喘组患儿在急性发作期及缓解期分别行荧光定量PCR（FQ-PCR）检测粪便双歧杆菌、大肠埃希菌;采用流式细胞术检测外周血Th1、Th2细胞水平;采用酶联免疫吸附试验（ELISA）检测外周血INF-γ、IL-4、TGF-β1水平并与对照组比较,从免疫角度分析肠道菌群紊乱与儿童支气管哮喘的关系。

对照组、哮喘组缓解期、哮喘组急性期患儿粪便双歧杆菌、B/E值依次降低,外周血Th1细胞、Th1/Th2值、INF-γ、TGF-β1水平依次降低,Th2细胞、IL-4水平依次升高,组间差异均有统计学意义（均P＜0.05）。哮喘组与对照组对象双歧杆菌、B/E值与Th1细胞、Th1/Th2、INF-γ、TGF-β1水平呈正相关,与Th2细胞、IL-4水平呈负相关（均P＜0.05）。

儿童支气管哮喘的发病与Th1/Th2细胞免疫失衡有关,肠道菌群失衡尤其是双歧杆菌数量的下降可引起Th2免疫应答亢进以及Th1免疫应答的抑制,从而引起支气管哮喘。

     

One functional variant in the 3′-untranslated region of TLR4 is associated with the elevated risk of ventilator-associated pneumonia in the patients with chronic obstructive pulmonary disease

The aim of this study was to identify the association polymorphism (rs11536889) in the 3′-untranslated region (3′-UTR) of Toll-like receptors 4 (TLR4) and the risk for ventilator-associated pneumonia (VAP). miRNA database online and luciferase assays were used to validate TLR4 as the target gene of miR-1236. Enzyme-linked immunosorbent assay analysis and western blot were used to analyze the level of TLR4 in different genotype groups. In the present study, miR-1236 was predicted to bind to the rs11536889 G allele rather than the rs11536889 C allele, which was further confirmed by the luciferase activity suppressed by a fragment of 3′-UTR containing the rs11536889 G allele induced by lipopolysaccharide (LPS) and interleukin-6 (IL-6). Bronchial epithelial cells isolated from participants genotyped as GG, GC, and CC, with no remarkable difference in TLR4 messenger RNA (mRNA) levels were observed among these genotype groups. After stimulating by LPS, a TLR4 ligand, the CC-genotyped cells expressed higher levels of IL-8, IL-6, and tumor necrosis factor alpha (TNF-α) on their surfaces than cells with the other genotypes. Finally, the western blot analysis results showed that the expression level of IL-8, IL-6, and TNF-α protein was much higher in the CC group than the GC and GG groups subsequent to stimulation by LPS, and the IL-8, IL-6, and TNF-α protein levels in the GC were grouped much lower compared with the GG group. These findings indicated the regulatory association of miR-1236 with TLR4 and the abnormal expression of TLR4 caused by the presence of rs11536889 in the 3′-UTR of mRNA, which interfere with its interaction with the miR-1236, contributing to the risk of VAP.     

支气管哮喘患者疾病认知状况调查及控制水平的影响因素分析

目的:调查支气管哮喘患者疾病认知状况,并分析控制水平的影响因素。方法:选取2018年7月~2020年7月期间贵州医科大学附属医院诊治的支气管哮喘患者100例,采用面对面问卷调查的方式调查所有患者疾病认知状况。采用哮喘控制测试(ACT)对患者哮喘控制水平进行评估。根据ACT结果将患者分为哮喘未控制组(n=57)和哮喘控制组(n=43)。分析哮喘控制水平的影响因素。结果:支气管哮喘患者对疾病认知相关问题的回答正确率均在60%以上,但仅有12%的患者使用过峰流速仪。本研究中100例患者均完成ACT,其中完全控制17例,控制良好26例,未控制57例,分别占比17.00%、26.00%、57.00%,哮喘控制率为43.00%。由单因素分析显示,支气管哮喘患者的哮喘控制水平与性别、家庭月收入、文化程度、家族史、吸烟史、居住处是否空气污染、病程、哮喘用药依从性、使用吸入性糖皮质激素治疗、抑郁情况、焦虑情况有关(P<0.05)。多因素Logistic回归分析显示:焦虑情况、抑郁情况、居住处空气污染、吸烟史是支气管哮喘患者哮喘控制水平的危险因素,而哮喘用药依从性、使用吸入性糖皮质激素治疗是支气管哮喘患者哮喘控制水平的保护因素(P<0.05)。结论:支气管哮喘患者对疾病有一定的正确认知,但仍未达到理想状态。哮喘控制水平受多种因素影响,可根据相关影响因素做出针对性的干预措施,以改善支气管哮喘控制水平。     

Interleukin-17A genetic variants can confer resistance to brucellosis in Iranian population

On the subject of brucellosis, it seems that Th1/Th2 cytokines balance may be involved in the resistance or susceptibility to Brucella infection. In this respect, Th1 cytokines confer resistance, while Th2 cytokines predispose brucellosis. It is also clarified that IL-17 is required for the induction of IFN-γ and IL-12 in macrophages and dendritic cells. Then, it seems that IL-17 can affect the induction of Th1 immunity which is necessary for controlling Brucella. In the present study, we tried to investigate probable relationship between IL-17A genetic variants and susceptibility to the human brucellosis. One hundred and seventy six patients with brucellosis and 84 healthy animal husbandmen, who consumed contaminated raw milk and dairy products from animals with brucellosis, were included in this study. All individuals were genotyped for 9 single nucleotide polymorphisms (SNPs) (rs4711998AG, rs8193036CT, rs3819024AG, rs2275913AG, rs3819025AG, rs8193038AG, rs3804513AT, rs1974226AG and rs3748067AG) being selected by using NCBI SNP database and literature using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. The distribution of IL-17 rs4711998, rs8193038, rs3748067 AA genotypes and AAGAA haplotype were significantly more frequent in the patients than in the controls (P = 0.008, 0.0019, 0.003 and 0.002, respectively) while IL-17 genotypes rs3819024GG and rs3819025AA were more frequent in the controls than the patients (P = 0.001 and 0.0035, respectively). Based on the results, IL-17 rs4711998, rs8193038, rs3748067 AA genotypes and AAGAA haplotype could be considered as susceptibility factors for brucellosis while the inheritance of IL-17 rs3819024GG and rs3819025AA genotypes might be resistance factors against the disease.     

Effect of endothelin antagonism on the production of cytokines in eosinophilic airway inflammation

Endothelin (ET)-1 has been launched as an important mediator in bronchial asthma, which is an eosinophilic airway inflammation. However, the interplay between ET-1 and other proinflammatory mediators during the development of airway inflammation has not been elucidated. We wanted to study 1) whether the production of ET-1 precedes the production of other proinflammatory mediators and 2) whether ET-1 stimulates the production of these mediators within the airways. These hypotheses were studied during the development of an eosinophilic airway inflammation in rats. The increase in ET-1 mRNA level in lung tissue preceded the increase in mRNA levels of tumor necrosis factor-alpha, interleukin (IL)-1beta, and IL-8. Treatment of the animals with the ET receptor antagonist bosentan resulted in a substantial decrease in the concentrations of tumor necrosis factor-alpha, IL-4, IL-1beta, interferon-gamma, and ET-1 in bronchoalveolar lavage fluid. In conclusion, the synthesis of ET-1 as measured by increased mRNA level precedes the synthesis of other proinflammatory cytokines of importance for the development of an eosinophilic airway inflammation, and ET antagonism inhibits the production of these mediators within the airways. Whether treatment with ET antagonists will prove beneficial for patients with eosinophilic airway inflammations like bronchial asthma is not yet known.     

支气管哮喘患儿血清25 羟维生素D3水平对病情评估及临床转归的意义

目的：探讨支气管哮喘患儿血清25 羟维生素D3[25-(OH)D3］水平对病情严重程度及临床转归的影响。方法：选取144 例 支气管哮喘患儿为研究对象,依据病情严重程度分为轻度间歇组、轻度持续组、中度持续组及重度持续组,选取60 例健康儿童作 为对照组,检测血清25-(OH)D3 水平;在治疗4 周后应用儿童哮喘控制测试评分系统(C-ACT)对患儿哮喘控制情况给予评价,将 所有患儿分为未控制组、部分控制组及完全控制组,比较各组血清25-(OH)D3 水平的差异。结果：对照组、轻度间歇组、轻度持续 组、中度持续组、重度持续组5 组之间血清25-(OH)D3 水平存在显著的统计学差异(P＜0.05),从对照组到重度持续组血清25- (OH)D3 水平逐渐降低(P＜0.05);完全控制组、部分控制组及未控制组三组血清25-(OH)D3 水平亦存在显著的统计学差异(P＜ 0.05),从完全控制组到未控制组血清25-(OH)D3 水平亦呈现逐渐降低趋势(P＜0.05);血清25-(OH)D3 水平与病情严重程度呈负 相关(rs =-0.489, P＜0.05),血清25-(OH)D3 水平与C-ACT 评分亦呈负相关(rs =-0.470, P＜0.05);随着血清25-(OH)D3 水平下降 程度的加重,患儿发生重度持续发作、出现C-ACT 评分＜19 分的风险值(OR)则逐渐增大。结论：血清25-(OH)D3 水平与哮喘患儿 病情严重程度及病情控制情况密切相关,早期血清维生素D 水平对于哮喘患儿病情及近期预后具有一定意义。     

Capsaicin induces the production of IL-6 in human upper respiratory epithelial cells

Capsaicin, a type of alkaloid and the pungent component of chili peppers, is used as a therapeutic drug against allergic rhinitis and also as an index of bronchial hypersensitivity. Capsaicin receptor (TRPV1) expression has been identified in non-neuronal cells as well as neuronal cells. In our previous study, both TRPV1 protein and its gene expression on nasal epithelial cells were confirmed by immunohistochemistry and RT-PCR, respectively. In order to clarify whether or not TRPV1 acts as a functional receptor, we examined the effects of capsaicin on the production of IL-6 from primary cultured human airway epithelial cells at both protein and mRNA levels. Human nasal epithelial cells (HNECs) and normal human bronchial/tracheal epithelial cells (NHBE cells) were stimulated with increasing concentrations of capsaicin and/or pretreatment with capsazepine (TRPV1 antagonist) at 37 degrees C. The supernatant and total RNA were collected at 0, 4, 12, 24 and 48 h after treatment. IL-6 concentration and the IL-6 mRNA level were evaluated by ELISA and real-time PCR, respectively. Capsaicin (10 nM-10 muM) induced production of IL-6 from HNECs and NHBE cells and this effect was inhibited by pretreatment with capsazepine. Our findings suggest that topical application of capsaicin to the airway induces IL-6 production from respiratory epithelial cells via activation of TRPV1.     

布地奈德联合孟鲁司特钠治疗支气管哮喘的有效性和安全性及对肺功能的影响

为了探讨布地奈德联合孟鲁司特钠治疗支气管哮喘的有效性和安全性及对肺功能的影响,并探讨IL-23/IL-17轴在发病过程中的作用,本研究首先通过卵清蛋白(ovalbumin,OVA)给药诱导支气管哮喘大鼠实验模型,对大鼠分别应用布地奈德、孟鲁司特钠、布地奈德+孟鲁司特钠治疗,采用RT-PCR和免疫组化染色检查大鼠肺组织中IL-23和IL-17的表达。然后,将80例支气管哮喘患儿随机分为观察组和对照组,每组40例,观察组采用布地奈德联合孟鲁司特钠治疗,对照组采用布地奈德治疗,两组均治疗1周。比较两组治疗后的疗效、肺功能指标(呼吸频率,潮气量,达峰时间比(TPEF/VE)和达峰容积比(VPEF/VE))和炎症因子(IL-1β,IL-6,IL-17,IL-23和TNF-α)水平。研究显示,哮喘模型大鼠肺组织病变严重且IL-17和IL-23均为高表达(p<0.05)。布地奈德联合孟鲁司特钠对肺组织病理的改善效果更明显,且极大地抑制了IL-23/IL-17轴的激活。支气管哮喘患儿治疗后,观察组的有效率(95.00%)显著高于对照组(82.50%)。观察组的呼吸频率显著低于对照组,而潮气量、达峰时间比和达峰容积比均显著高于对照组(p<0.05)。观察组患儿的炎症因子水平均显著低于对照组(p<0.05)。本研究表明,在治疗支气管哮喘患儿过程中,布地奈德联合孟鲁司特钠通过抑制IL-23/IL-17轴的激活来抑制炎症因子的表达,从而改善了患者的肺功能并提高了治疗效果。     

Association between Polymorphism of the Interleukin-13 Gene and Susceptibility to Hepatocellular Carcinoma in the Chinese Population

ObjectiveInterleukin-13 (IL-13) is a potent pleiotropic cytokine that is produced by activated CD4 T cells. This study was undertaken to determine the relationship between two IL-13 gene single nucleotide polymorphisms (SNP rs1800925 and SNP rs20541) and the incidence of hepatitis B virus-related (HBV) hepatocellular carcinoma (HCC).MethodThree hundred and ninety-eight HBV-positive individuals (192 HCC and 206 patients with chronic hepatitis) and one hundred and ninety-two healthy participants from the First Affiliated Hospital of Guangxi Medical University were enrolled in this study.ResultsThe results showed no significant differences between the genotype and allele frequencies of the IL-13 gene rs1800925 and rs20541 polymorphisms and chronic hepatitis B risk after adjusting for age, sex, tobacco use, and alcohol intake using binary logistic regression analyses. Regarding the rs20541 SNP, the GA genotype was significantly related to a decreased risk of HCC after adjusting for age, sex, tobacco use, and alcohol intake using binary logistic regression analyses (The odds ratio (OR) = 0.54, 95% confidence intervals (CI) 0.34–0.87). The adjusted OR for the GA and AA genotypes combined was 0.68 (95% CI 0.39–0.90).ConclusionThis study indicates that the functional IL-13 rs20541 polymorphism may contribute to the risk of HCC and that the rs20541 polymorphism is a protective factor for HCC.     

Genome-wide association study of bronchial asthma in the Volga-Ural region of Russia

Bronchial asthma is a chronic inflammatory respiratory disease that is caused by the complex interaction of environmental influences and genetic susceptibility. The first genome-wide association study of bronchial asthma discovered a significant association between SNPs within 17q12-21 genomic region and childhood bronchial asthma in individuals of European descent. Association with this genomic region was then replicated in a number of independent samples of European and Asian descent. Here we report results of the first genome-wide association study of bronchial asthma in the Volga-Ural region of Russia. The present study includes 358 unrelated patients with physician-diagnosed bronchial asthma and 369 disease-free control subjects of different ethnic origin (Russians, Tatars and Bashkirs). Genotyping of DNA samples was carried out using the Illumina Human610 quad array as a part of GABRIEL project (contract from the EC No LSHB-CT-2006-018996). After QC filtering procedures, a final set of 550915 SNPs genotyped in 330 cases and 348 controls was tested for association with bronchial asthma. Five markers on chromosome 17q12-21 showed statistically significant association with bronchial asthma (p < or = 4.79 x 10(-7)). SNP rs7216389 with the strongest evidence for association (p = 1.01 x 10(-7)) is located within the first intron of the GSDMB gene. Evidence for association was stronger with childhood-onset asthma (p = 1.97 x 10(-6) for SNP rs7216389) compared to late-onset asthma (p = 1.8 x 10(-4) for SNP rs7216389). Our replication study using three SNPs within GSDMB gene confirmed association with only childhood-onset asthma. In summary, these results suggest an important role for genetic variants within 17q12-q21 region in the development of bronchial asthma in the Volga-Ural region of Russia.     

Effects of catalpol on bronchial asthma and its relationship with cytokines

An animal (BALB/c mice) model of catalpol associated with bronchial asthma in vivo was established, and the effects of catalpol and its relationship with cytokines were investigated. A total of 30 adult BALB/c mice were randomly divided into a positive control group, a model group, and a catalpol group, with 10 mice in each group. The lung function of mice, the cell count, and the cytokine concentrations in bronchoalveolar lavage fluid (BALF) were detected. The levels of cytokines [interleukin 4 (IL-4), interleukin 5 (IL5), and interferon gamma (IFN-γ)] in BALF were measured with enzyme-linked immunosorbent assay methods. The total number of cells in the BALF of the group treated with catalpol was significantly lower than the model group. After treatment with catalpol, the eosinophils and neutrophils of the mice were remarkably reduced compared with the model group. The malondialdehyde content in the lung tissue homogenate of the mice was also decreased in the catalpol group. The cytokines IL-5 and IL-4 exhibited a similar tendency: the concentrations of IL-4 and IL-5 for the catalpol group were dramatically decreased compared with the model group. However, the IFN-γ concentration for the catalpol group was higher than the model group. The results indicated that IL-5 may involve in the pathologic process of asthma-like IL-4, and an inflammatory reaction may still exist in the airway during the remission stage of asthma. The imbalances of the cytokine network might be an important molecular basis in the asthma pathogenesis. It is suggested that catalpol may be a potential drug for the clinical treatment of asthma.