支气管哮喘患者血清骨桥蛋白和嗜酸细胞趋化因子表达及临床意义

支气管哮喘是慢性气道炎症性疾病,嗜酸性粒细胞在气道炎症反应中起重要作用[1]。现认为细胞因子网络失衡是发病的基础,而Th2细胞因子、嗜酸细胞趋化因子(eotaxin)共同诱导的嗜酸性粒细胞募     

类胰蛋白酶及其与支气管哮喘的关系

类胰蛋白酶是与胰蛋白酶有关的另一类丝氨酸蛋白酶 ,主要由肥大细胞表达和储存。由于类胰蛋白酶具有四聚体晶体的特殊结构 ,其生化和生物学特征与胰蛋白酶及其他蛋白酶家族又有所区别。类胰蛋白酶通过形成四聚体 ,在组织中获得酶活性 ,并通过裂解一些关键蛋白、活化一些具有广泛特异性的蛋白酶、刺激细胞反应 ,导致气道高反应、慢性气道炎症和气道重建 ,在支气管哮喘发病过程中起重要作用。     

三氧化二砷减轻支气管哮喘小鼠气道重塑及基质金属蛋白酶-9表达

气道重塑是支气管哮喘的典型特征之一,主要因气道壁结构的改变,形成不可逆的气流阻塞和持续性气道高反应,导致肺功能下降,故预防和逆转哮喘的气道重塑具有重要意义.     

支气管哮喘患者的血液流变性特征

支 气管哮喘 (哮喘 )是一种气道慢性炎症性疾病。它与一般急性感染性炎症不同 ,主要因炎症细胞浸润、释放介质 ,导致支气管高反应性 ,平滑肌收缩。为了探讨哮喘患者的血液流变性特征 ,我们对哮喘稳定期门诊患者进行了血液流变学检测 ,现报告如下。1　资料与方法1.1　对象哮喘组 :34例均为哮喘稳定期门诊患者。男 19例、女15例。年龄 2 1～ 6 9岁 ,平均 47.1± 15 .5岁。诊断符合中华医学会哮喘诊断标准[1] 。均服用茶碱类、β2 受体兴奋剂及吸入必可酮等治疗。无高脂血症及高血糖 ,肝肾功能正常。近4周内无急性上、下呼吸道感染。对照组 :34…     

支气管哮喘患者血清嗜酸细胞阳离子蛋白的变化

探讨检测血清嗜酸细胞阳离子蛋白在支气管哮喘的诊断１病情监测及疗效判断中的价值。方法采用荧光酶免疫法测定了发作期和缓解哮喘患者各２０例,慢性阻塞性肺疾病患者１６例和正常人２０例的血清ＥＣＰ,同时进行了肺功能测定,并对发作期哮喘患者在给予吸入皮质激素治疗３ｍｏ后复测其ＥＣＰ及肺。     

支气管哮喘小白鼠支气管肺泡灌洗液中TGF-β含量的变化

气道重构 (airwayremodeling)是难治性支气管哮喘气道发生不可逆性气流阻塞及持续性非特异性气道高反应性的重要原因之一。TGF β是分子量约 2 5kD的蛋白质 ,最近报道TGF β具有刺激纤维母细胞促进纤维结合素及胶原的等间质成分的产生[1 ] ,于是推测TGF β在支气管哮喘气道重构中可能起重要的作用。在国内定量性研究TGF β在支气管哮喘气道重构中的作用尚无文献报道。本实验用小白鼠建立支气管哮喘气道重构的动物模型测定 (bronchoalveollarlavageflu id ,BALF)中TGF β的含量阐明气道重构中它的作用。1　材料与方法1 1　动物 :动物…     

支气管哮喘患者外周血T细胞亚群的表达及临床分析

支气管哮喘是以气道高反应性和可逆性气流受阻为特征的慢性气道炎症性疾病。很多细胞参与该炎症过程,其病理基础是多种炎症性细胞（肥大细胞、嗜酸性粒细胞、巨噬细胞、中性粒细胞、淋巴细胞等）及自细胞介素等细胞因子和黏附分子的相互调控下释放炎症介质引起支气管平滑肌收缩、微血管渗漏,黏液腺分泌增加以及直接损伤气道上皮甚至剥脱,并导致气道高反应性发生的病理基础,气道高反应性是支气管哮喘的特征。其中T淋巴细胞及其分泌的细胞因子在哮喘的发病过程中发挥着重要的免疫调节作用。     

杏丁注射液对支气管哮喘患者血液流变性的影响

目的 观察杏丁注射液治疗支气管哮喘急性发作期对血液流变性的影响。方法 将47例支气管哮喘患者随机分为治疗组22例，对照组25例。对照组按常规治疗，治疗组在常规治疗基础上给予杏丁注射液20ml 5％葡萄糖液(GS)250ml静脉滴注，每日1次，14d为一疗程。结果 杏丁注射液治疗后全血高切黏度、低切黏度、血浆黏度、红细胞比容等指标较治疗前明显下降，与常规治疗有明显差异，临床疗效的改善与血液流变性改善一致。结论 杏丁注射液可显著改变血液流变状态，并能提高支气管哮喘的临床疗效。     

128例支气管哮喘患者的过敏原检查结果分析

支气管哮喘的发病与变态反应有关,已被公认的主要为I型变态反应。它由嗜酸性细胞、肥大细胞和T淋巴细胞等多种炎性细胞参与的气道慢性炎症,这种炎症使易感者对各种激发因子具有气道高反应性,并可引起气道缩窄。     

从“培土生金”论治支气管哮喘脾肺两虚证患者的效果及对气道高反应性及细胞免疫功能的影响

目的:探讨"培土生金"论治支气管哮喘(Bronchial Asthma,BA)脾肺两虚证患者的效果及对气道高反应性及细胞免疫功能的影响.方法:将我院2018年8月至2021年2月期间119例BA脾肺两虚证患者按照计算机随机分组法分为对照组59例,给予常规治疗,观察组60例在对照组基础上给予"培土生金"法(自拟健脾益肺汤)治疗,观察两组临床疗效、气道高反应性、肺功能、微炎症状态以及细胞免疫功能.结果:治疗后,观察组总有效率(93.33％)高于对照组(79.66％)(P<0.05);观察组气道传导率低于对照组,第一秒最大呼气量(Forced Expiratory Volume In One Second,FEV1)、FEV1/用力肺活量(Forced Vital Capacity,FVC)水平高于对照组(P<0.05);观察组肿瘤坏死因子-α(Tumor Necrosis Factor-α,TNF-α)、白细胞介素-17(Interleukin 17,IL-17)、白细胞介素-6(Interleukin 6,IL-6)水平低于对照组(P<0.05);观察组CD4+、CD4+/CD8+水平低于对照组,CD8+水平高于对照组(P<0.05).结论:从"培土生金"法论治BA脾肺两虚证患者可改善微炎症状态,缓解气道高反应性以及改善细胞免疫功能和肺功能,进而提高治疗效果.     

Eosinophil activity markers in peripheral blood have high predictive value for bronchial hyperreactivity in patients with suspected mild asthma

The present study aimed to evaluate the predictive value of eosinophils and markers of their activity for bronchial hyperreactivity (BHR) in a population of patients with recently developed clinical symptoms of asthma. The activation of eosinophils was estimated by measuring eosinophil cationic protein (ECP) in serum. In addition, flow cytometry was used to measure the expression of the EG2-epitope on intracellular ECP in eosinophils from peripheral blood. Twenty-eight consecutive patients with clinical history of asthma were studied. Of the 28 patients, 18 had a positive bronchial challenge test measured as PD₂₀≤ 1600 μg histamine. A significantly higher concentration of eosinophils and a trend to higher ECP in the peripheral blood was found in the hyperreactive group than in the nonreactive group. However, the intracellular expression of ECP did not correlate with the PD₂₀ value, and no significant difference between the groups was found. With one eosinophil activity marker, either serum ECP or EG2, BHR could be predicted in 70% of the patients. If we combined any two of the activity markers (serum ECP, EG2, or the percentage of eosinophils), the predictive value increased to 100%. We conclude that the blood eosinophil concentration, as well as, to some extent, serum ECP, has a high specificity for BHR in patients with recently developed clinical symptoms of asthma. Despite normal bronchial reactivity, some patients had signs of activated eosinophils, i.e., high serum ECP and increased EG2 expression. Thus, these markers may reflect early stages in the development of BHR. Our results also indicate that a combined evaluation of percentage of eosinophils and of eosinophil activity markers is of clinical value to predict BHR.     

抗原特异性IgG在支气管哮喘中作用的初步研究

目的探讨抗原特异性IgG在支气管哮喘免疫学发病机制中的作用.方法复制采用通气功能作为判定指标的小鼠实验性支气管哮喘模型,用间接ELISA方法检测哮喘小鼠血清中特异性IgG、IgE,通过IgG与通气功能指标-气道阻力等的相关性检验,初步分析IgG在支气管哮喘中的作用.结果支气管哮喘小鼠血清中特异性IgG增高(t=4.537,P＜0.05),IgG与气道阻力呈负相关(r=-0.708,0.02＜P＜0.05),与IgE虽无明显相关, 但有负相关倾向(r=-0.452,0.10＜P＜0.20).结论初步分析认为抗原特异性IgG对支气管哮喘发作起抑制作用.     

Hyperresponsiveness of bronchial but not tracheal smooth muscle in a murine model of allergic bronchial asthma

Objective: To determine a change in airway smooth muscle contractility in a murine model of allergic asthma, the responsiveness of airway smooth muscles isolated from ovalbumin (OA)-sensitized and -challenged mice was compared with that from control animals.Methods: Actively sensitized mice were repeatedly challenged by ovalbumin (OA) antigen inhalation. Twenty-four h after the last antigen challenge, tracheal and bronchial smooth muscle responsiveness to acetylcholine (ACh) and endothelin-1 (ET-1) were measured. Airway microvascular leakage and histochemistry were also determined as indices of airway inflammation.Results: Both the ACh and ET-1 responsiveness of bronchial, but not tracheal, smooth muscles were significantly augmented in OA-challenged mice, whereas no significant change in the expression levels of M₂, M₃ and ET_B receptors was observed. The Evans blue dye extravasation in the main bronchial, but not tracheal, tissue of OA-challenged mice was significantly increased as compared with that of sensitized control animals. A marked inflammatory cells infiltration was also observed in bronchial but not tracheal tissues of OA-challenged mice.Conclusion: Repeated antigen challenge to sensitized mice caused a hyperresponsiveness of bronchial, but not tracheal, smooth muscle accompanied with bronchial tissue inflammation.Received 22 April 2004; returned for revision 10 June 2004; accepted by M. Katori 9 July 2004     

Tissue inhibitor of metalloproteinase-1 modulates allergic lung inflammation in murine asthma

Matrix metalloproteinases (MMPs) modulate development, inflammation, and repair in lungs. Tissue inhibitors of MMPs (TIMPs) interact with MMPs, controlling the intensity and nature of the response to injury. Absence of MMP-9, -2, and -8 activities is associated with altered lung inflammation during allergic sensitization. To test the hypothesis that the absence of TIMP-1 enhances allergic lung inflammation, airway hyperreactivity (AHR), and lung remodeling in asthma, we studied TIMP-1 null (TIMP-1 KO) mice and their WT controls using an ovalbumin (OVA) asthma model. TIMP-1 KO mice, compared to WT controls, developed an asthma phenotype characterized by AHR, pronounced cellular lung infiltrates, greater reduction in lung compliance, enhanced Th2 cytokine mRNA and protein expression, and altered collagen lung content associated with enhanced MMP-9 activity. Our findings support the hypothesis that TIMP-1 plays a protective role by preventing AHR and modulating inflammation, remodeling, and cytokine expression in an animal model of asthma.     

Association between − 308 tumour necrosis factor promoter polymorphism and bronchial hyperreactivity in asthma

BACKGROUND: Tumour necrosis factor (TNF) is a pivotal cytokine in the inflammation underlying asthma. The TNF gene is located in the polymorphic HLA class 3 region on chromosome 6p. Several polymorphisms in this region have been described and associated with alteration of TNF secretion in vitro. OBJECTIVE: In this study we tested the hypothesis that two such polymorphisms, lymphotoxin alpha NcoI B*1 and -308 TNF2 may be components of the genetic predisposition to asthma. METHODS: Five hundred and fifty-six random individuals were studied, comprising approximately equal numbers of asthmatic subjects, with or without atopy, and a nonatopic nonasthmatic control group. In addition, 355 subjects (172 asthmatics) from 60 multiplex families were typed at the LTalpha NcoI locus. RESULTS: There was an association between allele two of the -308 TNF polymorphism and bronchial hyperreactivity (OR 2.12, 95% CI 1.04-4.32, P = 0.036). However, there was no association with LTalpha NcoI alleles. To determine whether this was influenced by linkage disequilibrium within the MHC, 91 subjects with bronchial hyperreactivity and 85 control subjects were typed for class 2 and 3 alleles. Following identification of the extended TNF2 haplotype, we found no independent association of these alleles with BHR. CONCLUSIONS: We conclude that the -308 TNF2 promoter polymorphism may form a component of the genetic predisposition to BHR in asthma.     

Effect of viewing a humorous vs. nonhumorous film on bronchial responsiveness in patients with bronchial asthma

The effect of viewing a humorous film on bronchial responsiveness to methacholine [methacholine study: 20 healthy participants and 20 patients with house dust mite (HDM)-allergic bronchial asthma (BA)] or to epigallocatechin gallate (EGCg; EGCg study: 15 normal participants and 15 EGCg-allergic BA patients) was studied. At baseline, bronchial challenge test to methacholine (20 normal participants and 20 HDM-allergic BA patients) or EGCg (15 normal participants and 15 EGCg-allergic BA patients) were performed. After 2 weeks, patients and healthy participants were randomly assigned to watch a humorous or a nonhumorous film. Two weeks later, the alternate film was watched. Immediately after viewing, bronchial challenge test to methacholine or ECGg to each study group were performed. Viewing a humorous film significantly reduced bronchial responsiveness to methacholine or EGCg, while viewing a nonhumorous film failed to do so in BA patients without affecting bronchial responsiveness to methacholine or EGCg in healthy participants. These findings indicate that viewing a humorous film may be useful in the treatment and study of BA.     

初诊哮喘患者的呼出气一氧化氮与大小气道功能的 相关性及临床价值分析

目的 探讨初诊支气管哮喘患者的呼出气一氧化氮水平与大小气道功能的相关性,以及在哮喘规范化治疗中的变化趋势及临床意义。方法 选择2016年3月~2016年5月就诊于新乡医学院第一附属医院呼吸科的初诊成人支气管哮喘患者80例,为哮喘组;选择同期健康体检志愿者40名,为对照组。哮喘组在治疗前及治疗后3、6、9、12月分别行FeNO和肺功能检查包括FEV1%、FEF75%、FEF50%、MMEF%以及哮喘控制测试（ACT）;健康志愿者仅行一次肺功能及FeNO检查。结果 初诊哮喘的FeNO与FEV1%无相关性（P＞0.05）,与FEF75%、FEF50%、MMEF%存在负相关（P＜0.05）。经治疗大气道功能的恢复时间6个月早于小气道功能的恢复时间12个月,FeNO的恢复时间约3月。小气道功能异常的哮喘患者比小气道功能正常者具有更高的FeNO,且在1年的治疗过程中具有更高的急性发作次数和吸入糖皮质激素（ICS）用量,差异有统计学意义（P＜0.05）。结论 相比于大气道,小气道功能异常与气道炎症FeNO的关系更密切。大气道功能不能完全反映哮喘的临床控制情况,需联合检测FeNO与小气道功能。     

Effect of pranlukast on bronchial inflammation in patients with asthma

BACKGROUND: Pranlukast (8-[p-(4-phenylbutyloxy) benzol] amino-2-[tetrazol-5-yl]-4-oxo-4H-1-benzopyran hemihydrate), a selective cysteinyl leukotriene receptor antagonist, has been reported to exhibit not only antileukotrine activity but also pharmacological activity including antieosinophilic effects. OBJECTIVE: This study was designed to investigate whether the antiasthmatic activity of pranlukast is associated with a reduction in eosinophilic inflammation. METHODS: A double-blind, randomized, crossover design was used. Subjects received 225 mg of pranlukast or placebo orally twice daily for 4 weeks and then, after a washout period of at least 4 weeks, crossed over to receive the alternative treatment. We assessed the effects of pretreatment with pranlukast on bronchoconstriction precipitated by inhalation of methacholine in 32 adult patients with mild or moderate bronchial asthma; those who were in stable clinical condition were allocated to this study. Blood and sputum samples were taken the morning of the methacholine provocation test. Eosinophil counts and measurement of eosinophilic cationic protein (ECP) were performed. RESULTS: After the 4 weeks of treatment with pranlukast, patients' symptoms, blood eosinophils, serum ECP, sputum eosinophils, and sputum ECP were significantly decreased. Furthermore, values of PC20-methacholine significantly improved in the treatment with pranlukast. CONCLUSION: Our results suggest that pranlukast has an anti-inflammatory effect on bronchial eosinophilic infiltration. This study raises further interesting therapeutic possibilities and argues for further trials of new approaches to the treatment of bronchial asthma.