诱导痰嗜酸粒细胞与慢性持续期支气管哮喘病情严重程度的关系

目的观察初诊不同病情严重程度慢性持续期支气管哮喘（简称哮喘）患者的诱导痰嗜酸粒细胞（eosinophil,EOS）比例变化,探讨二者之间的关系,并分析诱导痰EOS比例与肺功能的相关性。方法收集专科门诊就诊的63例初诊慢性持续期哮喘患者,根据症状分为轻度持续、中度持续、重度持续3组,分别予诱导痰和肺功能检查。观察不同病情严重程度的患者气道炎症状况。对所得数据用SPSS 15．0软件分析,各组间总体分析采用Kruskal—wallis法,两组间分析采用Mann-Whitney U test法。结果①慢性持续期患者诱导痰EOS比例随病情严重程度增加呈增高趋势,重度持续患者诱导痰EOS比例显著高于轻度持续患者（41．8％vs17．8％,P=0．033）,但轻度持续与中度持续、中度持续与重度持续患者之间比较诱导痰EOS比例差异无统计学意义（P〉0．05）;②诱导痰EOS比例与第1秒用力呼气容积差异无统计学意义（r=-0．111,P〉0．05）,与第1秒用力呼气容积／用力肺活量（％）差异无统计学意义（r=-0．154,P〉0．05）。结论慢性持续期哮喘患者病情严重程度与诱导痰EOS比例有关,但症状不能完全反映气道炎症程度。评价哮喘患者的严重程度时应结合临床症状和气道炎症程度综合考虑。     

诱导痰嗜酸性粒细胞与慢性持续期哮喘病情严重程度的关系

目的观察并探讨初诊不同病情严重程度慢性持续期哮喘患者的诱导痰嗜酸性粒细胞(Eos)比例变化,以及诱导痰Eos比例与肺功能的相关性。方法收集专科门诊就诊的63例初诊慢性持续期哮喘患者,根据症状分为轻度持续、中度持续、重度持续3组,分别予诱导痰和肺功能检查。观察不同病情严重程度的患者气道炎症状况。对所得数据用SPSS15.0软件分析,各组间总体分析采用Kruskal-Wallis法,两组间分析采用Mann-Whitney U法。采用Spearman rank-order法分析Eos比例与肺功能的相关性。结果①慢性持续期患者诱导痰Eos比例随病情严重程度增加呈增高趋势,重度持续患者诱导痰Eos比例显著高于轻度持续患者(41.8%vs17.8%,P=0.033),但轻度持续与中度持续、中度持续与重度持续患者之间比较诱导痰Eos比例均无显著差异(P0.05);②诱导痰Eos比例与FEV1无显著相关(r=-0.111,P0.05),与FEV1/FVC(%)无显著相关(r=-0.154,P0.05)。结论慢性持续期哮喘患者病情严重程度与诱导痰Eos比例有关,但症状不能完全反映气道炎症程度。评价哮喘患者的严重程度时应结合临床症状和气道炎症程度综合考虑。     

EOS、总IgE与儿童哮喘严重程度和肺功能的相关性

目的 分析血嗜酸性粒细胞(EOS)、总IgE与儿童哮喘严重程度和肺功能的相关性。方法 选择2018年1月至2021年1月我院收治并确诊的55例支气管哮喘患儿,根据病情严重程度分为轻度组18例、中度组22例、重度组15例。对比不同病情严重程度组儿童血清EOS、总IgE、FeNO及肺功能第1秒用力呼气容积占预测值百分比(FEV₁%pred)、呼气峰值流速(PEF)和用力肺活量(FVC)水平变化;观察给予吸入性糖皮质激素(ICS)治疗前后,哮喘组儿童上述指标变化情况;采用Spearman秩相关和Pearson相关性分析血清EOS、总IgE与儿童哮喘FeNO、病情严重程度及肺功能的相关性。结果 哮喘组儿童FeNO及血EOS%、总IgE水平升高,肺功能指标FEV₁%pred、PEF、FVC明显降低(P<0.05);重度哮喘组上述指标高于/低于中度组,中度组高于/低于轻度组(P<0.05)。ICS治疗后,哮喘组儿童FeNO及血EOS%、总IgE水平较治疗前降低,肺功能指标升高,治疗前后差异有统计学意义(P<0.05)。儿童哮喘血EOS%...     

支气管哮喘患者ICAM-1、EOS水平与病情严重程度的相关性分析

目的分析支气管哮喘患者细胞间黏附分子-1(ICAM-1)、嗜酸性粒细胞(EOS)水平与症状严重程度及肺功能的相关性。方法选取2018年1月至2018年2月我院行肺功能检查者400例,其中支气管哮喘病例65例,纳入哮喘组,肺部病变者300例,纳入非哮喘组,健康体检者35例,纳入对照组,比较三组诱导ICAM-1、血清中EOS水平及肺功能检查结果[每分钟最大通气量(MVV)/预计值、第一秒用力呼气容积(FEV_1)、呼气峰流速值(PEF)、用力肺活量(FVC)],比较不同症状严重程度哮喘患者血清ICAM-1、EOS、肺功能检查结果,并分析其相关性。结果哮喘组ICAM-1、EOS水平高于非哮喘组、对照组(P0.05);哮喘组MVV/预计值、FEV_1、PEF、FVC明显低于非哮喘组、对照组(P0.05);重度哮喘者ICAM-1、EOS水平高于轻、中度者,而MVV/预计值、FEV_1、PEF、FVC低于轻、中度者,轻、中度哮喘者MVV/预计值、FEV_1、FVC比较差异也有统计学意义(P0.05);相关性分析显示,支气管哮喘患者ICAM-1、EOS水平与FEV_1、FVC呈负相关(P0.05)。结论支气管哮喘患者ICAM-1、EOS水平与其症状严重程度及肺功能存在密切关系,参与气道炎症反应,对临床诊治有一定价值。     

诱导痰气道炎症指标与支气管哮喘病情关系的探讨

目的 探讨气道炎症指标对支气管哮喘(简称哮喘)患者病情监测及治疗的意义.方法 收集2004年1月至2006年1月在北京大学第三医院呼吸科门诊就诊的近半年来未使用口服或吸入激素治疗的哮喘患者87例.进行哮喘症状评分、肺功能检查、诱导痰上清液检测白介素-8(IL-8)浓度及嗜酸粒细胞阳离子蛋白(ECP)浓度,对所有患者病情分级状况和气道炎症指标进行分析,探讨病情严重程度与气道炎症之间的关系;分析急性发作与气道炎症之间的关系.结果 (1)重度哮喘患者中性粒细胞、IL-8水平较轻中度患者明显增高;(2)急性发作期患者嗜酸性粒细胞(EOS)、ECP较缓解期明显增高;(3)中性粒细胞与第1秒用力呼气量(FEV1)呈负相关(r=-0.522,P＜0.05);中性粒细胞与IL-8呈正相关(r=0.832,P＜0.05);(4)ECP、EOS与FEV1、症状评分均无相关性(r=-0.209,r=-0.189,P均＞0.05;r=-0.289,r=-0.229,P均＞0.05);ECP与EOS呈正相关(r=0.852,P＜0.01);(5)中性粒细胞对重度哮喘的阳性预测值为91%,EOS对哮喘急性发作的阳性预测值为92.5%,ECP对哮喘急性发作的阳性预测值98.5%.结论 (1)中性粒细胞、IL-8与病情严重程度有关,重度哮喘患者中性粒细胞、IL-8明显增高;(2)ECP、EOS与哮喘的急性发作有关,急性发作期哮喘患者ECP、EOS明显增高;(3)气道炎症指标可用于监测哮喘病情和调整哮喘治疗.     

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.     

哮喘患者诱导痰中TARC、MDC水平变化及糖皮质激素对其影响

目的探讨胸腺活化调节趋化因子(TARC)及巨噬细胞衍生趋化因子(MDC)在哮喘中的作用及评价哮喘发作严重程度方面的临床价值。方法选择35例慢性持续期哮喘患者(轻中度组20例、重度组15例)及20例健康体检者(对照组),ELISA法检测诱导痰内TARC、MDC水平,痰涂片计数嗜酸性粒细胞百分比(EOS%);测定肺功能,记录1秒钟用力呼气量占预计值的百分比(FEV1%pred),分析TARC、MDC、EOS%、FEV1%pred之间的相关性。结果治疗前轻中度、重度哮喘组诱导痰TARC、MDC水平均高于对照组(P<0.01),重度组TARC水平高于轻中度组(P<0.05);诱导痰TARC水平与MDC、EOS%呈正相关;MDC与EOS%呈正相关,与FEV1%pred呈负相关;轻中度、重度哮喘组治疗后TARC水平较治疗前降低(P<0.05)。结论 TARC的水平可作为哮喘患者临床病情判定和疗效观察的良好指标,吸入糖皮质激素至少部分是通过降低TARC水平减轻气道炎症反应;MDC可能与哮喘气道炎症的慢性持续过程有关。     

动态监测哮喘患者诱导痰嗜酸性粒细胞的临床意义

目的　探讨利用诱导痰中嗜酸性粒细胞 (EOS)评价哮喘患者气道炎症变化的方法 ,为如何相对准确监测哮喘患者气道炎症的改变提供临床实验资料。方法　分别对 2 8例哮喘患者(哮喘组 ,其中轻度组 15例、中度组 13例 )、16例回访者 (哮喘回访组 )和 14例健康自愿者 (对照组 )进行痰的诱导 ,所有检查者通过超声雾化吸入浓度为 4%～ 5 %的高渗盐水 3 0min ,选取诱导出的痰栓 ,用 0 .1%的二硫苏糖醇处理 ,单盲法计数EOS。结果　哮喘组诱导痰EOS数占炎性细胞百分比高于对照组 ,哮喘轻度组与中度组EOS数占炎性细胞百分比比较差异无显著性 (P >0 .0 5 ) ,哮喘回访组缓解前后EOS比较差异有非常显著性 (P <0 .0 1)。结论　单纯一次EOS计数值不能说明患者病情的轻重 ,但对同一患者动态监测其发病过程中诱导痰EOS的变化可以在一定程度上反映其病情改变     

慢性持续期支气管哮喘患者治疗后气道炎症表型变化分析

目的 研究慢性持续期支气管哮喘患者治疗后气道炎症表型变化。方法 采用回顾性研究的方法，选取2018年1月至2021年12月就诊于山西医科大学第一医院呼吸与危重症医学科门诊初次确诊为哮喘且行诱导痰检测的患者343例，其中在治疗后5年内行1次及以上诱导痰检测的患者33例。分析慢性持续期哮喘患者治疗前和治疗后气道炎症表型分布、治疗后气道炎症表型变化及肺通气功能变化。结果 共获取33例患者的105份痰液，首次行诱导痰时气道炎症表型分布为中性粒细胞(neutrophil, NEU)型6例(18.2%),嗜酸性粒细胞(eosinophil, EOS)型16例(48.5%),混合细胞(mixed cell, MIX)型10例(30.3%),寡细胞(paucigranulocytic, PAU)型1例(3.0%),即气道炎症表型以EOS型为主；治疗后5年内行诱导痰检测，24/33例患者气道炎症表型发生了改变，其气道炎症表型分布为NEU型30例(41.7%),EOS型20例(27.8%),MIX型16例(22.2%),PAU型6例(8.3%),即气道炎症表型以NEU型为主。治疗3月后诱导痰EOS%下降，...     

白细胞介素-32与慢性阻塞性肺疾病患者肺功能损害的相关性

目的探讨白细胞介素(IL)-32与慢性阻塞性肺疾病(COPD)患者肺功能损害的相关性。方法选取正常人30例,COPD急性加重期(AECOPD)患者30例。AECOPD组接受布地奈德混悬液2 mg雾化吸入,3次/d,治疗1 w。收集正常人及AECOPD患者治疗前后痰液和静脉血,酶联免疫吸附试验(ELISA)检测痰液和血清中IL-32蛋白的表达。检测正常人及AECOPD患者治疗前后肺功能,分析COPD患者IL-32浓度与肺功能损害的相关性。结果 AECOPD组痰液及血清中IL-32浓度明显升高(P0.05),治疗后血清IL-32浓度较治疗前明显降低(P0.05);IL-32浓度与第1秒用力呼气容积(FEV1)占预计值百分比[FEV1(%)]、第1秒用力呼气量占用力肺活量比值(FEV1/FVC)及氧合指数呈负相关关系。结论 IL-32诱导COPD气道炎症,使肺功能损害加重;布地奈德能有效抑制IL-32的表达,起到控制气道炎症、改善肺功能的作用。     

Clinical assessment of asthma severity partially corresponds to sputum eosinophilic airway inflammation

In the aim to evaluate the relationship between sputum eosinophil percentages and eosinophil cationic protein (ECP) concentrations, as markers of airway inflammation, and different Levels of asthma severity, we examined 223 patients consecutively observed in our asthma clinic. Diagnosis of asthma was made according to internationally accepted criteria. Asthma severity was evaluated according to frequency of symptoms, FEV1, peak expiratory flow variability and level of asthma treatment needed to control asthma. Spontaneous or induced sputum was collected. Adequate sputum samples were obtained in 68 untreated subjects and in 117 subjects regularly treated with ICS. A control group of 14 normal subjects was also examined. In untreated subjects, mild intermittent asthmatics showed a lower sputum eosinophil percentage in comparison with other groups of asthma severity, while no difference in ECP levels was detected. In treated subjects, severe asthmatics showed higher levels of sputum eosinophils and ECP in comparison with other groups of asthma severity. Mild persistent and moderate persistent patients did not differ for sputum eosinophils or ECP in both untreated and treated subjects. Controls were significantly different from all groups of untreated and treated asthmatics. In conclusion, the assessment of asthma severity according to clinical and functional findings only partially corresponds to the severity of eosinophilic airway inflammation as assessed by induced sputum analysis.     

Reduced eosinophil apoptosis in induced sputum correlates with asthma severity.

This study was carried out to investigate the relationship between induced sputum eosinophil apoptosis and clinical severity score, airway obstruction and symptom scores in patients with chronic stable asthma. Altogether, 41 chronic stable asthmatic subjects of varying severity defined by Aas score and 17 control subjects underwent spirometry, symptom questionnaire and successful sputum induction. Sputum was processed and cytospins prepared for light microscopy to determine normal and apoptotic eosinophils. Mild asthmatic subjects had a significantly lower percentage sputum eosinophils and a significantly higher eosinophil apoptotic ratio (AR) than moderate or chronic severe asthmatics. Severe asthmatic subjects had a significantly greater age, duration of asthma and sputum eosinophil count x mL(-1) than mild asthmatic subjects. Asthmatic subjects' symptom scores, severity scores and age inversely correlated with AR and the percentage of sputum eosinophils. Baseline forced expiratory volume in one second inversely correlated with percentage sputum eosinophils and positively correlated with AR. The study demonstrates a relationship between reduced sputum eosinophil apoptosis and increased clinical severity of chronic stable asthma, providing additional evidence that eosinophil apoptosis may be important in the resolution of eosinophilic airway inflammation in asthma.     

The relationship between airways inflammation and asthma severity

In order to investigate the relationship between airways inflammation and disease severity, and improve the understanding of persistent asthma, 74 asthmatics, with disease severity ranging from intermittent, to mild to moderate and severe persistent (classified according to the Global Initiative for Asthma [GINA] guidelines), and 22 nonatopic control subjects were studied using the method of induced sputum. Sputum was analyzed for total and differential cell counts concentrations of albumin, and levels of eosinophil cationic protein (ECP), myeloperoxidase (MPO), and tryptase, inflammatory mediators reflecting eosinophil, neutrophil, and mast cell activation. Asthma severity (assessed by FEV(1), peak expiratory flow [PEF] variability, and daily symptom scores) and methacholine airways responsiveness were related to sputum eosinophilia and ECP. In addition, sputum neutrophilia and MPO levels correlated, albeit weakly, with PEF variability and symptom scores, respectively. Tryptase concentrations were raised in mild to moderate asthmatics. Albumin concentrations were significantly raised across the spectrum of asthma severity and correlated with those of tryptase and ECP. Despite treatment with either high doses of inhaled corticosteroids or oral corticosteroids, prominent eosinophilic inflammation with raised ECP was noted. This study points to persistent, disease severity-related airways inflammation in asthma, involving eosinophils, mast cells, and neutrophils, which is evident despite treatment with corticosteroids.     

Eosinophil soluble protein levels, eosinophil peroxidase and eosinophil cationic protein in asthmatic patients.

Eosinophil granular proteins are useful eosinophil activation markers in asthmatic patients. In this study, eosinophil peroxidase (EPO) and eosinophil cationic protein (ECP) levels were assessed in different stages of bronchial asthma in 123 patients suffering from intrinsic (n = 42) and extrinsic (n = 81) asthma, with the aim of evaluating the difference in the protein levels between both types of asthma and their importance as a severity marker of the disease. The geometric mean serum level of EPO was 12.3 +/- 2.17 ng/ml (mean +/- SD) in controls, and 38.6 +/- 3.4 ng/ml in the asthmatic patients. Mean ECP levels were 13.22 +/- 1.11 ng/ml in controls and 30.5 +/- 2.38 ng/ml in patients. Depending on the asthma severity, the EPO levels were 30.4 +/- 4.35, 38.7 +/- 5.29, and 54.46 +/- 9.46 ng/ml in mild, moderate and severe asthmatics, respectively, with the differences being significant between the groups of patients with mild and severe asthma (p < 0.001). ECP levels were 24.23 +/- 3.37 in mild, 31.69 +/- 4.21 in moderate, and 37.61 +/- 4.52 ng/ml in severe asthma. There were significant differences in ECP levels between mild and moderate asthma (p < 0.001) and between mild and severe asthma (p < 0.001). Peripheral eosinophil count was 157 +/- 20 eosinophils/mm3 in controls, 334 +/- 35 eosinophils/mm3 in mild asthmatics, 510 +/- 87 eosinophils/mm3 in moderate asthmatics and 658 +/- 72 eosinophil/mm3 in severe asthmatics, with significant differences between all groups (p < 0.05-p < 0.001). Serum EPO and ECP levels and peripheral eosinophil count were significantly greater in patients with active asthma than in patients with silent asthma (p < 0.001). Significant negative correlations (p < 0.001) were found between serum EPO levels and FEV1 (rs = -0.30), MEF25-75 (rs = -0.33), MEF50 (rs = -0.34). There was also a significant (p < 0.001) and negative correlation between ECP levels and FEV1 (rs = -0.31), MEF25-75 (rs = -0.31), MEF50 (rs = -0.32). A good positive correlation was found between peripheral eosinophil count and EPO levels (rs = 0.80, p < 0.001), and ECP levels (rs = 0.67, p < 0.001). We also found a significant positive correlation between clinical score and peripheral eosinophil count (rs = 0.54, p < 0.001), EPO levels (rs = 0.46, p < 0.001) and ECP levels (rs = 0.52, p < 0.001).     

Induced sputum in adolescents with severe stable asthma. Safety and the relationship of cell counts and eosinophil cationic protein to clinical severity.

This study examined the safety of sputum induction and the relation between sputum cell counts and clinical parameters in adolescents with severe persistent asthma. Within 5 days, induced sputum and reversibility in forced expiratory volume in one second (FEV1), quality of life, provocative concentration causing a 20% fall in FEV1 (PC20) of adenosine monophosphate and histamine, exercise-induced bronchoconstriction, overall asthma severity index, and blood eosinophils were collected in 20 atopic adolescents with moderate-to-severe persistent asthma (12-18 yrs of age, FEV1 65-110% of predicted, on 500-2,000 microg inhaled steroids daily). FEV1 was reversible by 13.3-2.3% pred. After sputum induction, FEV1 was still increased by 9.0+/-2.6% pred as compared to the pre-salbutamol baseline. Sputum contained, median (range): 12.4 (0.4-59.5)% squamous cells, 47.3 (6.8-84.0)% macrophages, 39.0 (4.6-84.8)% neutrophils, 4.8 (1.0-12.4)% lymphocytes, 0.4 (0-10.8)% eosinophils and 3.6 (0-23.4)% bronchial epithelial cells. Sputum eosinophils showed a trend towards a significant association with the overall asthma severity index (r=0.46, p=0.06) and correlated inversely with baseline FEV1 (r=-0.51, p=0.03). In conclusion, sputum can be induced safely in adolescents with moderate-to-severe persistent asthma, if pretreated with beta2-agonists. Despite relatively low sputum eosinophil counts in these patients on inhaled steroids, the association of eosinophil numbers with baseline forced expiratory volume in one second and asthma severity index favours a role of induced sputum in monitoring adolescents with severe asthma.     

支气管哮喘患者诱导痰中基质细胞衍生因子的表达及其作用

目的 测定支气管哮喘(简称哮喘)患者在糖皮质激素(简称激素)治疗前后诱导痰中基质细胞衍生因子-1(SDF-1)和白细胞介素(IL)-17的水平,探讨SDF-1在哮喘发病机制中的作用.方法 收集2009年6月至2010年9月郑州大学第一附属医院门诊及住院的慢性持续期的哮喘患者99例(按病情严重程度分为轻、中、重度组)及健康体检者30名,哮喘患者在回答哮喘控制问卷(ACQ)后,两组研究对象分别进行肺功能检测和诱导痰检查,记录FEV1占预计值%,行诱导痰炎症细胞分类计数,酶联免疫吸附试验(ELISA)法检测诱导痰中SDF-1和IL-17水平;所有哮喘患者均参照支气管哮喘指南给予规范的吸入激素为主的治疗,4周后测定诱导痰中SDF-1、IL-17的水平及炎症细胞比率.结果 轻、中、重度持续组的ACQ评分及FEV1占预计值%差异均有统计学意义(F值分别为79.271和457.448,均P<0.01).治疗前哮喘组诱导痰嗜酸粒细胞比率、IL-17水平及SDF-1水平均高于健康对照组(均P<0.01);重度哮喘患者诱导痰中两种炎症细胞比率及SDF-1和IL-17水平均高于轻度哮喘患者(均P<0.05).哮喘患者FEV1占预计值%与诱导痰中嗜酸粒细胞、中性粒细胞比率均呈负相关(r值分别为-0.316和-0.409,均P<0.05);诱导痰中SDF-1与嗜酸粒细胞比率及中性粒细胞比率呈正相关(r值分别为0.875和0.716,均P<0.01);诱导痰中IL-17与嗜酸粒细胞及中性粒细胞比率呈正相关(r值分别为0.878和0.846,均P<0.01);诱导痰中SDF-1与IL-17水平呈正相关(r=0.872,P<0.01).治疗后哮喘患者诱导痰中两种炎症细胞比率及SDF-1和IL-17水平均低于治疗前患者(均P<0.01);治疗后未控制组哮喘患者诱导痰中性粒细胞比率、SDF-1水平和IL-17水平明显高于完全控制组(均P<0.05).结论 SDF-1和IL-17通过募集炎症细胞,特别是中性粒细胞参与了哮喘气道炎症的发生,SDF-1可作为哮喘患者临床病情判定和疗效观察的参考指标.

Abstract：

Objective To evaluate concentrations of stromal cell-derived factor 1 (SDF-1) and IL-17 in induced sputum supernatants from asthmatic patients before and after treatment with glucocorticosteroids. Methods Induced sputum was collected from 30 healthy controls and 99 patients with chronic persistent asthma from 2009-2010. Sputum samples were obtained before and after 4 week treatment with inhaled glucocorticosteroids. The sputum concentrations of SDF-1 and IL-17 were measured by ELISA. Results The FEV1% and the asthma control score of patients with severe asthma were decreased as compared with patients with moderate persistent and mild persistent asthma (F=457.448 and 79.271, all P<0.01). The concentrations of SDF-1 ,IL-17 and the percentage of eosinophils were increased in asthma group compared with control subjects (all P<0.01),but the percentage of sputum neutrophils was lower than that in the healthy controls(P<0.01). The percentage of sputum neutrophils and eosinophils and the level of SDF-1 and IL-17 in patients with severe persistent asthma were significantly higher than those in patients with mild persistent asthma (all P<0.05). The percentage of sputum neutrophils and eosinophils were negatively correlated with FEV1%(r=-0.409 and -0.316,all P<0.05). The levels of IL-17 and SDF-1 were positively correlated with the percentage of sputum neutrophils and eosinophils (all P<0.01). The levels of IL-17 were positively correlated with the levels of SDF-1(r=0.872, P<0.01).After glucocorticosteroid therapy, the percentage of eosinophils and neutrophils, the levels of IL-17 and SDF-1 decreased significantly in all patients(all P<0.01), while the percentage of sputum neutrophils and the levels of IL-17and SDF-1 in uncontrolled patients increased significantly compared with the controlled and partly controlled groups(all P<0.05). Conclusions SDF-1 and IL-17 may contribute to airway inflammation in asthma by chemotactic activity towards neutrophils. The concentration of SDF-1 may be used to evaluate the inflammation and the therapeutic effects.     

哮喘患者诱导痰中IL-17A、IL-8及MMP-9水平变化及糖皮质激素对其的影响

目的探讨哮喘患者气道炎症特点及糖皮质激素的作用机制。方法将33例哮喘患者（哮喘组）按病情程度分为轻、中度19例及重度14例,予规范吸入糖皮质激素治疗4周,行诱导痰炎性细胞分类并计数,采用ELISA法检测痰上清液炎性介质白细胞介素-17A（IL-17A）、IL-8、基质金属蛋白酶-9（MMP-9）水平,并与15例查体健康者（对照组）进行比较。对诱导痰细胞分类、1秒钟用力呼气量占预计值百分比（FEVl％）及炎性介质水平进行相关分析。结果重度哮喘者诱导痰中性粒细胞、嗜酸性粒细胞比值及上清液IL-17A、IL-8、MMP-9水平显著高于对照组及轻、中度者;轻-中度者除MMP-9无显著升高外,余各指标均显著高于对照组（P均〈0．01）。诱导痰中性粒细胞及嗜酸性粒细胞比值与FEV1％呈显著负相关;中性粒细胞比值与IL-8、MMP-9呈正相关;IL-17A水平与中性粒细胞比值、IL-8呈正相关。糖皮质激素治疗后重度者中性粒细胞、嗜酸性粒细胞比值及MMP-9水平仍显著高于轻-中度者。结论中性粒细胞浸润性气道炎症是重度持续性哮喘的重要特征;IL-17A、IL-8与MMP-9可能在其中发挥重要作用。吸入糖皮质激素能抑制炎症细胞的趋化效应,阻止炎症释放,稳定细胞溶酶体膜,减轻组织损伤。