支气管哮喘与气道炎症和支气管高反应性

现已普遍认为支气管哮喘是一种气道炎症（ＡＩ）疾病，支气管高反应性（ＢＨＲ）是其重要特征。本探讨了哮喘与ＡＩ和ＢＨＲ的关系，进而阐述哮喘的可能发病机制。     

支气管哮喘与气道炎症和支气管高反应性

现已普遍认为支气管哮喘是一种气道炎症(AI)疾病,支气管高反应性(BHR)是其重要特征。本文探讨了哮喘与AI和BHR的关系,进而阐述哮喘的可能发病机制。     

肺炎支原体感染与小儿支气管哮喘的关系

采用微量颗粒血清凝集沉淀方法．检测103例哮喘急性发作期患儿和30例非感染性疾病患儿静脉血中肺炎支原体（MP）特异性抗体IgM（MP—IgM）滴度及血清总IgE含量，并观察大环内酯类抗生素疗效。结果哮喘组MP-IgM阳性率为44．66％，对照组阳性率为6．67％，两者差异有统计学意义（P〈0.05）;MP—IgM阳性的哮喘患儿血清IgE含量明显高于阴性患儿，差异有统计学意义。认为MP感染与儿童哮喘关系密切，大环内酯娄抗牛素疗效确切，可降低短期哮喘发作率。     

气道变应性炎症与支气管哮喘

本文概述了气道变应性炎症和支气管哮喘的气道通气障碍、气道高反应性和迟发性哮喘反应之间的密切关系,据此并提出了哮喘发病机理和治疗的新概念。     

气道炎症介质受体和支气管哮喘

气道内肥大细胞释放的炎症介质,是引起支气管哮喘病理生理改变的主要因素。这些炎症介质通过激活气道靶细胞表面的特异性受体,引起细胞反应而导致发病。开发特异性介质拮抗剂对于哮喘的临床治疗可能具有重要意义。     

支气管哮喘与小气道炎症的研究进展

支气管哮喘是常见的慢性呼吸道疾病之一,患病率在全球范围内有逐年增加趋势.1922年Hubert和Koessler第1次描述了重症哮喘存在气道重塑[1].2002年,全球哮喘防治创意(GINA)提出,无论轻重度哮喘,大小气道均存在急性和慢性炎症,各级气道都存在气道重塑.近年来,哮喘的小气道炎症研究受到学术界的广泛重视,国内外在哮喘与小气道炎症方面进行了大量研究.我们就哮喘小气道炎症进展作一综述.     

儿童咳嗽变异性哮喘与反复肺炎支原体感染的相关性研究

目的探讨儿童咳嗽变异性哮喘(CVA)与反复肺炎支原体(MP)感染的相关性。方法选择2014年1月至2016年3月我院住院的CVA患儿60例为A组,MP感染患儿60例为B组,同期以咳嗽为主要症状的反复上呼吸道感染60例患儿为对照组C组。3组患儿均行肺炎支原体抗体(MP-IgM)检测,比较各组中MP阳性率及MP阳性与年龄及性别的相关性,同时观察3组患儿血清总IgE水平及血嗜酸粒细胞(EOS)计数的差异性。结果 (1)A组和C组的MP-IgM阳性率分别为43.33%和23.33%,A组MP-IgM阳性率明显高于对照组(P0.05)。年龄越大,CVA患儿的MP-IgM阳性率越高。男童MP-IgM阳性率高于女童;(2)A、B两组外周血EOS及血清总IgE水平明显高于对照组(P0.05);(3)ROC曲线示,EOS曲线下面积为0.860,最佳阈值为1.08×10~9/L,敏感度为0.852,特异度为0.780;总IgE曲线下面积为0.776,最佳阈值为196.53IU/mL,敏感度为0.795,特异度为0.834;结论 MP感染与小儿CVA有密切相关性,可以将MP-IgM检测作为CVA患儿的常规筛查项目,EOS及总IgE对CVA具有较高的预测价值。     

Distribution of airway inflammation phenotype in patients with bronchial asthma and its correlation with control level

<正>Objective To investigate the distribution of airway inflammation phenotypes in patients with bronchial asthma and its correlation with asthma control level. Methods Patients who met GINA 2017 asthma diagnostic criteria from October 2017 to April 2018 in respiratory outpa-     

支气管哮喘气道炎症可能机制的探讨

目的 探讨支气管哮喘(简称哮喘)患者气道炎症特征及其可能机制,并进一步观察吸入糖皮质激素治疗对气道炎性细胞分类计数、炎症介质等的影响.方法 分别选择轻度(轻度组)、中度(中度组)和重度(重度组)持续哮喘患者15例、14例和19例,正常对照组15名,分别行哮喘症状控制评分、肺功能测定、诱导痰炎性细胞分类计数、调节激活正常T细胞表达和分泌细胞因子(RANTES)、嗜酸粒细胞阳离子蛋白(ECP)、白介素8(IL-8)及髓过氧化物酶(MPO)浓度检测,然后规范吸人糖皮质激素治疗4周,随访复查上述指标.结果 诱导痰NEU%、IL-8及MPO重度组明显升高,分别为(62.40±22.05)%、594.53±85.11、39.25±10.67与轻度组[(47.23±15.12)%、183.63±120.98、12.47±4.15]、中度组[(46.13±19.23)%、352.76±71.72、22.93±7.35]、正常对照组[(31.44±13.31)%、103.26±36.33、10.22±4.13]比较差异均有统计学意义(P＜0.01);RANTES、嗜酸粒细胞百分比(EOS%)和ECP浓度在各哮喘组间比较差异无统计学意义(P＞0.05).EOS%与RANTES、ECP水平呈正相关(r=0.557,P＜0.05;r=0.852,P＜0.01);NEU%与IL-8、MPO水平呈正相关(r=0.732,P＜0.05;r=0.806,P＜0.05);经糖皮质激素治疗后,对轻、中、重度哮喘患者合并进行分析表明,治疗后症状评分由(9.8±5.4)分下降至(4.0±3.5)分和肺功能指标第一秒用力呼气容积占预计值百分比由(62.2±23.3)%升高至(75.9±17.5)%显著改善,差异有统计学意义(P＜0.01).在接受糖皮质激素治疗后,RANTES、EOS%和ECP水平均显著降低.另外MPO水平也显著降低(P＜0.01);但治疗后在重度组仍显著高于轻、中度组(P＜0.01).但IL-8、NEU%治疗后无明显降低(P＞0.05),而且治疗后IL-8、NEU%在重度组仍显著高于轻、中度组(P＜0.01).结论 中性粒细胞增多是重度哮喘的气道炎症特征之一,EOS与病情严重程度无关.EOS哮喘的发生可能与RANTES的趋化、EOS的活化、ECP的释放有关,激素可以抑制EOS气道炎症.而中性粒细胞哮喘的发生可能与IL-8的趋化、NEU的活化、MPO的释放有关.     

支气管哮喘气道炎症可能机制的探讨

目的探讨支气管哮喘（简称哮喘）患者气道炎症特征及其可能机制,并进一步观察吸入糖皮质激素治疗对气道炎性细胞分类计数、炎症介质等的影响。方法分别选择轻度（轻度组）、中度（中度组）和重度（重度组）持续哮喘患者15例、14例和19例,正常对照组15名,分别行哮喘症状控制评分、肺功能测定、诱导痰炎性细胞分类计数、调节激活正常T细胞表达和分泌细胞因子（RANTES）、嗜酸粒细胞阳离子蛋白（ECP）、白介素8（IL～8）及髓过氧化物酶（MPO）浓度检测,然后规范吸入糖皮质激素治疗4周,随访复查上述指标。结果诱导痰中性粒细胞百分比、IL-8及MPO重度组明显升高,分别为（62．40±22．05）％、594．53±85．11、39．25±10．67与轻度组[（47．23±15．12）％、183．63±120．98、12．47±4．15]、中度组[（46．13±19．23）％、352．76±71．72、22．93±7．353、正常对照组[（31．44±13．31）％、103．26±36．33、10．22±4．13]比较差异均有统计学意义（P〈O．01）;RANTES、嗜酸粒细胞百分比（EOS％）和ECP浓度在各哮喘组间比较差异无统计学意义（P〉0．05）。EOS％与RANTES、ECP水平呈正相关（r=0．557,P〈0．05;r=0．852,P〈0．01）;中性粒细胞百分比与IL-8、MPO水平呈正相关（r=0．732,P〈0．05;r=0．806,P〈0．05）;经糖皮质激素治疗后,对轻、中、重度哮喘患者合并进行分析表明,治疗后症状评分由（9．8±5．4）分下降至（4．0±3．5）分和肺功能指标第1秒用力呼气容积占预计值百分比由（62．2±23．3）％升高至（75．9±17．5）％显著改善,差异有统计学意义（P〈0．01）。在接受糖皮质激素治疗后,RANTES、EOSO和ECP水平均显著降低。另外MPO水平也显著降低（P〈0．01）;但治疗后在重度组仍显著高于轻、中度组（P〈0．01）。但IL-8、中性粒细胞百分比治疗后?     

支气管哮喘患者血清维生素D与气道炎症关系探讨

目的探讨血清维生素D浓度与支气管哮喘血清炎症因子及哮喘急性发作次数的关系。方法选取支气管哮喘患者200例,检测血清维生素D、IL-2及TNF-α浓度,记录近2年哮喘急性发作的次数,研究血清维生素D浓度与IL-2、TNF-α及哮喘急性发作次数的关系。结果支气管哮喘合并低维生素D患者占51.5%,其中合并低维生素D患者支气管哮喘急性发作次数及IL-2、TNF-α明显高于不合并低维生素D患者,差异有显著性(P<0.05)。结论血清维生素D与气道炎症、支气管哮喘急性发作次数密切相关。     

Effect of inhaled corticosteroids on small airway inflammation in patients with bronchial asthma

Bronchial asthma is a chronic inflammatory disease affecting the bronchial mucosa. In asthma patients, the highest number of inflammatory cells, including eosinophils, are found in the small bronchi. According to the most recent 2006 report of the Global Initiative for Asthma, inhaled corticosteroids (ICS) remain the first?line treatment of chronic asthma. They are characterized by high lung deposition and good distribution in the small bronchi, which makes them particularly efficient in reducing chronic inflammatory infiltrate in the small airways. Good pulmonary distribution of ICS in patients with mild asthma is reflected by a better control of the disease, improvement in the quality of life, improvement in the results of pulmonary function tests, decreased levels of exhaled proinflammatory nitric oxide, lower number of inflammatory cells (including eosinophils) in the induced sputum, decrease in bronchial hyperreactivity, and decrease in exhaled air trapping observed in the computed tomographic scanning of the lungs.     

Chlamydia pneumoniae infection and inflammation in adults with asthma

BACKGROUND: Chlamydia pneumoniae infection and immune response to the C. pneumoniae heat shock protein 60 (CpHsp60) have been suggested to be associated with asthma. OBJECTIVES: To study whether a slightly elevated C-reactive protein (CRP) level as a marker of low-grade systemic inflammation has a role in this association, we collected serum and sputum samples from 103 asthma patients with disease severity ranging from mild to moderate and from 30 healthy volunteers. METHODS: IgA and IgG antibodies to C. pneumoniae elementary bodies (CpEB) and CpHsp60 were measured by enzyme immunoassay. Serum CRP levels were measured with a rapid two-site ultra-sensitive assay based on time-resolved immunofluorometry. RESULTS: The asthma patients, especially those with moderate asthma, had higher serum IgA antibody levels to CpHsp60 than the healthy controls (test for trend, p = 0.05), whereas antibody levels to CpEB antigen did not differ between the study groups. CRP levels were higher in both asthma groups compared to the control group and moreover, the patients with moderate asthma had higher CRP levels than those with mild asthma (test for trend, p < 0.01). The subjects with a slightly elevated CRP level, defined as > or =1.8 mg/l, had higher CpEB IgA (p = 0.001), CpEB IgG (p = 0.008) and CpHsp60 IgA (p = 0.023) antibody levels in serum compared to the subjects with lower CRP levels. CONCLUSIONS: Slightly elevated CRP levels as a marker of low-grade systemic inflammation may be associated with C. pneumoniae infection in asthma patients.     

Roles of hyperresponsiveness and airway inflammation in bronchial asthma

Bronchial hyperresponsiveness is one important feature of bronchial asthma, and evidence has been accumulated that airway inflammation contributes to the specific airway response in asthmatic patients. Increase in airway responsiveness following viral infection, exposure to allergen, ozone or chemical sensitizers supports the evidence for a link between hyperresponsiveness and airway inflammation. However, as only some respiratory tract infections induce an increase in hyperresponsiveness, and patients with chronic bronchitis and cystic fibrosis have less airway hyperresponsiveness than asthmatics, airway inflammation is considered to be only one of many factors contributing to the hyperresponsiveness of asthmatic airways.     

Allergic bronchial asthma: airway inflammation and hyperresponsiveness

The international consensus report on diagnosis and treatment of asthma was published in 1992 (Clin Exp Allergy 22: 1-72). According to the report, asthma is a chronic inflammatory disorder of the airways in which many cells play a role, including mast cells and eosinophils. Airway inflammation causes various symptoms of asthma which are usually associated with widespread but variable airflow obstruction and causes an associated increase in airway responsiveness to a variety of stimuli. The definition of asthma, provided in this report, is an epoch-making revision of the conventional recognition of asthma based on respiratory physiology and does not contradict the empirical knowledge that asthma responds well to steroid therapy. One reason, which led airway inflammation to be understood as a major factor in the pathophysiology of asthma is the technological advance and the widespread use of bronchoscopes. The use of bronchoscopy as a research tool has markedly improved the understanding of the pathology of asthma. It became also possible to link biopsy findings to autopsy findings in patients who died of asthma. However, it is relatively difficult to repeat a biopsy of the airway mucosal membranes in individual asthmatic patients. Here, animal models of asthma play a significant role. Findings from animal models can provide a clue for the development of new anti-asthmatic drugs. This paper will deal with the paradigm of allergic asthma and focus on recent topics of interleukin (IL)-4 and IL-5, which seem to play a central role in allergic asthma. The causative relationship between airway inflammation and hyperresponsiveness will be discussed.     

Smoking and airway inflammation in patients with mild asthma.

STUDY OBJECTIVES: Cigarette smoking is common in asthmatic patients, and we investigated the impact of cigarette smoking on airway inflammation in asthma. DESIGN: Single-center observational study of airway inflammation in asthmatic and healthy smokers and nonsmokers. SETTING: Asthma research unit in a university hospital. PATIENTS OR PARTICIPANTS: Sixty-seven asthmatic and 30 nonasthmatic subjects classified as smokers or nonsmokers. Asthmatics had chronic, stable asthma and were not receiving inhaled or oral steroids at the time of the study. INTERVENTIONS: We examined induced-sputum cell counts and levels of interleukin (IL)-8 and eosinophilic cationic protein (ECP). Bronchial hyperreactivity was assessed using methacholine challenge. MEASUREMENTS AND RESULTS: Asthmatic smokers had higher total sputum cell counts than nonsmoking asthmatics and both smoking and nonsmoking healthy subjects. Smoking was associated with sputum neutrophilia in both asthmatics and nonasthmatics (median, 47% and 41%, respectively) compared with nonsmokers (median, 23% and 22%, respectively), and sputum IL-8 was increased in smokers compared with nonsmokers, both in subjects with asthma (median, 945 pg/mL vs 660 pg/mL, respectively) and in healthy subjects (median, 1,310 pg/mL vs 561 pg/mL, respectively). Sputum eosinophils and ECP levels were higher in both nonsmoking and smoking asthmatics than in healthy nonsmokers. In smoking asthmatics, lung function (FEV(1) percent predicted) was negatively related to both sputum IL-8 (r = - 0.52) and sputum neutrophil proportion (r = - 0.38), and sputum IL-8 correlated positively with smoking pack-years (r = 0.57) and percent neutrophil count (r = 0.51). CONCLUSIONS: In addition to the eosinophilic airway inflammation observed in patients with asthma, smoking induces neutrophilic airway inflammation; a relationship is apparent between smoking history, airway inflammation, and lung function in smoking asthmatics.     

Markers of airway inflammation and airway hyperresponsiveness in patients with well-controlled asthma.

In steroid-naive asthmatics, airway hyperresponsiveness correlates with noninvasive markers of airway inflammation. Whether this is also true in steroid-treated asthmatics, is unknown. In 31 stable asthmatics (mean age 45.4 yrs, range 22-69; 17 females) taking a median dose of 1,000 microg inhaled corticosteroids (ICS) per day (range 100-3,600 microg x day(-1)), airway responsiveness to the "direct" agent histamine and to the "indirect" agent mannitol, lung function (forced expiratory volume in one second (FEV1), forced vital capacity (FVC), peak expiratory flow (PEF)), exhaled nitric oxide (eNO), and number of inflammatory cells in induced sputum as a percentage of total cell count were measured. Of the 31 subjects, 16 were hyperresponsive to mannitol and 11 to histamine. The dose-response ratio (DRR: % fall in FEV1/cumulative dose) to both challenge tests was correlated (r=0.59, p=0.0004). However, DRR for histamine and DRR for mannitol were not related to basic lung function, eNO, per cent sputum eosinophils and ICS dose. In addition, NO was not related to basic lung function and per cent sputum eosinophils. In clinically well-controlled asthmatics taking inhaled corticosteroids, there is no relationship between markers of airway inflammation (such as exhaled nitric oxide and sputum eosinophils) and airway responsiveness to either direct (histamine) or indirect (mannitol) challenge. Airway hyperresponsiveness in clinically well-controlled asthmatics appears to be independent of eosinophilic airway inflammation.