超短波治疗对COPD患者诱导痰炎症介质的影响

目的:研究超短波对COPD患者气道炎症及肺通气功能的影响并探讨其作用机理.方法:将74例急性发作期COPD患者分为超短波治疗组42例和对照组32例.超短波治疗组除常规治疗外行超短波治疗10～14天,对照组行常规治疗.两组患者均在治疗前后分别检测诱导痰液中白介素8(IL-8)、肿瘤坏死因子α(TNF-α)以及肺通气功能指标用力肺活量(FVC)、一秒时间肺活量(FEV1.0).结果:与对照组比较,超短波治疗组治疗后痰液IL-8、TNF-α均显著降低(P＜0.05),FVC%pred、FEV1.0%pred明显升高(P＜0.05).IL-8含量与FEV1.0呈显著负相关(r=-0.88,P＜0.05),TNF-α含量与FEV1.0呈负相关(r=-0.75,P＜0.05).结论:超短波辅助治疗COPD具有减轻气道炎症、提高肺通气功能的作用.     

慢性阻塞性肺病患者血清TNF-α水平与肺功能的关系探讨

目的:探讨慢性阻塞性肺病(COPD)患者血清肿瘤坏死因子-α(TNF-α)水平与其肺功能各参数之间的相关性。方法:选择我院收治的COPD患者60例和健康体检者35例。采用ELISA方法测定COPD患者和健康体检者血清TNF-α,同时测量其肺功能指标。结果:COPD组急性加重期、稳定期及正常对照的血清TNF-α水平呈下降趋势,三组间比较存在显著性差异(P0.01)。COPD组急性加重期和稳定期患者的各项肺功能指标FEV1、FVC、FEV1/FVC和MMEF均明显低于对照组(P0.01),且稳定期患者各肺功能指标均明显高于急性加重期患者(P0.01)。血清TNF-α水平与FEV1、FVC、FEV1/FVC及MMEF均呈负相关(r=-0.586,-0.714,-0.527,-0.639,P0.05)。结论:TNF-α与COPD的气道炎症反应和发病过程有关,并对肺功能产生重要影响。     

慢性阻塞性肺疾病急性发作期外周血及痰中IL-8和TNF-α测定的意义

为探讨COPD患者急性发作期以及病情缓解后全身炎症和气道炎症的变化及二者的相关性。对 4 5例COPD急性发作期患者治疗前及 10～ 14d病情缓解后分别行血常规及肺功能检查测定FEV1 0 占预计值百分数 (FEV1 0 pre )、用ELISA法检测外周血浆和诱导痰液中IL 8和TNF α的水平 ,并记录诱导痰液中性粒细胞占白细胞百分比 (Neu/Leu % )。结果COPD急性发作时外周血浆及诱导痰液中Neu/Leu %、IL 8和TNF α均明显高于缓解后水平 (P均 <0 0 1) ,痰液Neu/Leu %、IL 8和TNF α与血浆Neu/Leu %、IL 8和TNF α水平无明显差异 (P均 >0 0 5 ) ,外周血及痰液TNF α与FEV1 0 pre无明显差异 (P均 >0 0 5 ),外周血IL 8与FEV1 0 pre有关 (r= 0 6 2 71,P <0 0 5 ) ,痰液Neu/Leu %、IL 8与FEV1 0 pre呈显著负相关 (r= 0 85 2 7,P <0 0 1)。痰液Neu/Leu %、IL 8与COPD气道阻塞密切相关 ,气道炎症与全身炎症无关     

病毒感染与COPD的关系及对气道炎症的影响

目的 探究临床病毒感染与慢性阻塞性肺疾病(COPD)发生的相关性及其对气道炎症的影响,为临床COPD治疗提供指导性意见.方法 选取2009年2月-2014年2月来我院就诊的慢性阻塞性肺疾病急性加重期患者79例作为研究A组,COPD稳定患者43例作为研究B组,再选用与A、B组性别、年龄等基础状况相同的正常患者28例作为正常组,采用ELISA分别测定三组患者呼吸合胞病毒(RSV)、单纯疱疹病毒(HSV)、腺病毒(ADV)、巨细胞病毒(CMV)等病毒感染特异性抗体IgM和IgG水平状况,同时根据病毒特异性抗体IgM检测结果及患者临床表现将加重期患者79例分为C组27例和D组52例.分别测定并分析两组患者治疗前后痰液中白介素8(IL-8)和肿瘤坏死因子α(TNF-α)水平状况.结果 研究A组病毒总阳性率(88.61％)和研究B组病毒感染总阳性率(72.09％)明显高于正常组病毒总阳性率21.43％(x2=45.338,17.443、P＜0.01),研究A组IgM阳性率(34.18％)高于正常组(x2=7.647、P＜0.01),研究A、B两组IgG阳性率高于正常组(x2=42.103,15.225、P＜0.01),两组患者痰液治疗前后IL-8和TNF-α水平显著降低(P＜0.05),治疗后C组IL-8下降差值比D组高(P＜0.01),两组间TNF-α水平差值变化无差异.结论 病毒感染,尤其是呼吸合胞病毒与COPD急性加重关系密切,并可以导致气道炎症状况加重.     

支气管哮喘患者血清IL-10、IL-5和ECP的变化及其意义

目的 通过对支气管哮喘患者和正常对照组的血清IL-10, IL-5和 ECP水平的测定以及相互关系的研究,探讨它们在支气管发病中的作用.方法 应用Pharmacia UniCAP系统和ELISA方法分别测定支气管哮喘患者和正常对照组的血清E CP和IL-10、IL-5水平.结果 正常对照组和发作期的支气管哮喘患者的 ECP水平分别为(3.97±2.13) μg/L和(21.76±12.08) μg/L.正常对照组,支气管哮喘ECP 升高组和支气管哮喘ECP正常组的血清IL-5水平分别为(10.90±4.41) pg/mL,(20.62± 15.7 4) pg/mL和(9.24±7.16) pg/mL.正常对照组和支气管哮喘ECP升高组之间IL-5水平有显著差异(P＜0.01),正常对照组和支气管哮喘ECP正常组之间IL-5水平无差异(P＞0.05) ,支气管哮喘ECP正常组和ECP升高组之间IL-5水平有显著差异(P＜0.01),ECP与IL-5 明显相关 ,两者之间的相关系数r=0.465(P＜0.01).正常对照组,支气管哮喘ECP升高组和支气管哮喘ECP正常组的血清IL-10水平分别为(38.28±15.17) pg/mL,(22.76±15.25) pg/mL 和(42.32±14.61) pg/mL,支气管哮喘ECP正常组和ECP升高组之间IL-10水平有显著差异( P＜0. 01).结论 支气管哮喘的发生与嗜酸粒细胞有密切的关系,ECP和IL-5可反映嗜酸粒细胞的活化程度,在支气管哮喘发作时嗜酸粒细胞处于激活状态,易于释放蛋白颗粒;IL-5对嗜酸粒细胞有调控作用.支气管哮喘组的血清IL-10水平较正常对照组低,提示支气管哮喘患者IL-10分泌减少,不能有效抑制炎症或促炎症细胞因子的合成及释放,亦即不能有效抑制炎症反应,可能是导致或加重气道炎症的原因之一.     

气道嗜酸性粒细胞增高与COPD加重

有证据表明部分COPD加重期气道嗜酸性粒细胞增高 ,其原因可能与病毒感染有关 ;了解COPD加重期气道嗜酸性粒细胞增高的发病机制 ,认识伴有嗜酸性粒细胞增高的气道炎症对临床治疗中是否选择糖皮质激素有一定价值 ,本文就这方面进展作一综述     

气道嗜酸性粒细胞增高与COPD加重

有证据表明部分COPD加重期气道嗜酸性粒细胞增高,其原因可能与病毒感染有关;了解COPD加重期气道嗜酸性粒细胞增高的发病机制,认识伴有嗜酸性粒细胞增高的气道炎症对临床治疗中是否选择糖皮质激素有一定价值,本文就这方面进展作一综述.     

支气管哮喘患者FeNO的表达及临床意义

目的:探讨不同呼出气一氧化氮(Fractional exhaled nitric oxide,FeNO)水平下支气管哮喘患者痰液、血液、肺功能检测等多个观察指标的表达特点,并分析在气道高反应性中的预测价值。方法:选取2017年1月至2019年5月于我院就诊的120例疑似支气管哮喘患者作为研究对象进行前瞻性分析,根据FeNO水平不同,将FeNO>49 ppb的42例患者列为高水平组,FeNO为26~49 ppb的33例患者为低水平组,FeNO≤25 ppb的45例患者为正常组。比较三组患者的基本临床资料、痰嗜酸性粒细胞、痰中性粒细胞、血嗜酸性粒细胞阳离子蛋白(Eosinophilic cationic protein,ECP)和免疫球蛋白E(Immunoglobulin E,IgE)以及第1s用力呼气容积(Forced expiratory volume at 1s,FEV1)、FEV1占预测值百分比(FEV1%Pred)、用力肺活量(Forced vital capacity,FVC)以及FEV1与FVC比值(FEV1/FVC)等肺功能检测结果进行统计分析。结果:经Spearman相关性分析显示,血IgE、ECP水平与FeNO水平呈正相关(r=0.615/0.629,P>0.01),FEV1%pred、FEV1/FVC与FeNO水平呈负相关(r=-0.494/0.789,P>0.01)。其中血IgE、ECP、FEV1%pred、FEV1/FVC对于预测支气管哮喘有一定的价值,而联合上述指标对于预测支气管哮喘的准确性最佳(AUC=0.920,P>0.01)。结论:不同FeNO水平支气管哮喘患者在临床表现中具有显著差异,在血IgE、ECP和肺功能FEV1%pred、FEV1/FVC指标检测的基础上增加FeNO可大大增加预测支气管哮喘的准确性。     

哮喘患者ET-1、TNF-α、GM-CSF RIA

哮喘是多种细胞,特别是以嗜酸性粒细胞、T淋巴细胞等多种炎性细胞参与的气道慢性炎症,是呼吸系统疾病中常见病和多发病.测定哮喘患者急性发作期及缓解期血浆内皮素(ET-1)、血清肿瘤坏死因子(TNF-α)、粒细胞-巨噬细胞集落刺激因子(GM-CSF)的水平变化,探讨三者在哮喘发病中的作用.     

肝素结合蛋白、1,25-二羟基维生素D3、白三烯B4及炎性指标与慢性阻塞性肺疾病急性加重期患者肺功能的相关性研究

目的 探讨肝素结合蛋白、1,25-二羟基维生素D3、白三烯B4及炎性指标与慢性阻塞性肺疾病急性加重期患者肺功能的相关性研究.方法 选取360例2016年4月至2017年5月期间到我院呼吸科诊治的COPD和AECOPD患者作为研究对象.其中COPD患者167例,作为稳定组,AECOPD患者193例,作为加重组.选取同期进行体检的健康人300例作为对照组.比较3组受试者HBP、1,25-(OH)2D3、LTB4、TNF-α、IL-8和IL-6水平.比较稳定组和加重组肺功能指标.分析HBP、1,25-(OH)2D3、LTB4、TNF-α、IL-8和IL-6与患者肺功能相关性.结果 稳定组、加重组患者HBP和LTB4水平显著高于对照组,1,25-(OH)2D3显著低于对照组,加重组患者HBP和LTB4水平显著高于稳定组,1,25-(OH)2D3显著低于稳定组(P<0.05).稳定组、加重组患者TNF-α、IL-8和IL-6水平显著高于对照组,加重组患者TNF-α、IL-8和IL-6水平显著高于稳定组(P<0.05).加重组患者各肺功能指标(FEV1% Pred、FEV1/Fvc%、MMEF% Pred、V50% Pred、V25%Pred)均显著高于稳定组(P<0.05).经过Pearson相关性分析,HBP、LTB4、TNF-α、IL-8、IL-6与患者肺功能呈负相关, 1,25-(OH)2D3与患者肺功能呈正相关.结论 HBP、1,25-(OH)2D3、LTB4及炎性指标与AECOPD患者肺功能指标密切相关,可以评估患者的病情严重程度,指导临床治疗.     

Diagnostic accuracy of sputum outcomes in chronic stable asthma

BACKGROUND: Asthma with non-remitting airflow obstruction may not always be differentiated from COPD with airway hyperreactivity. Many attempts have been made to find useful markers for the distinction between these two disorders. OBJECTIVE AND METHODS: In order to help the finding of a useful marker for the diagnosis of asthma in the population of patients with airway obstruction we analysed the diagnostic accuracy of sputum eosinophils and sputum ECP in 91 patients with asthma, 15 patients with chronic bronchitis, 32 patients with chronic obstructive pulmonary disease (COPD) and 20 controls subjects, by performing ROC analysis. RESULTS: Sputum eosinophils were above the normal range of our laboratory (0-3.7%) in 48 asthma patients and in six COPD patients, while sputum ECP (normal range < 85 microg/L) was high in 65 asthma patients, in 24 COPD patients and in nine chronic bronchitis patients. The ROC analysis revealed that sputum eosinophils count (AUC = 0.82) was more accurate than both sputum ECP levels (AUC = 0.56) (P < 0.0001) and beta2-reversibility (AUC = 0.53) (P = 0.0001) in differentiating asthmatic from non-asthmatic subjects (COPD, chronic bronchitis patients and normal subjects). The diagnostic accuracy of ECP was similar to that of bronchial reversibility (P = 0.76). When ROC analysis was performed by including only patients with airway obstruction (36 asthmatics with airway obstruction and COPD patients), both eosinophil count (AUC = 0.77) and beta2-reversibility (AUC = 0.66) were more accurate than ECP measurement (AUC = 0.39) in discriminating asthmatics from COPD patients (P < 0.00001 and P = 0.04, respectively). CONCLUSION: Sputum eosinophils seem to be valid markers for detecting asthma in a population of patients with airway obstruction. Moreover, the higher diagnostic accuracy of eosinophils in the sputum compared to sputum ECP and bronchial reversibility reinforces the role of cytological analysis of sputum in the diagnosis of chronic stable bronchial asthma.     

Soluble interleukin-5 receptor alpha is increased in acute exacerbation of chronic obstructive pulmonary disease

BACKGROUND: During chronic obstructive pulmonary disease (COPD) exacerbations (AE-COPD), an influx of eosinophils into the bronchial mucosa has been described. Eosinophilic cationic protein (ECP) and soluble interleukin-5 receptor alpha (sIL5Ralpha) are secreted by eosinophils and increased in eosinophilic airway diseases. METHODS: We studied ECP and sIL5Ralpha expression in patients with COPD compared to healthy controls and smokers and investigated a possible association to viral exacerbations of COPD. Expression of sIL5Ralpha in serum was analyzed by ELISA and ECP by the Uni-Cap system. Induced sputum from patients with COPD was analyzed for six different respiratory viruses by nested PCR. RESULTS: ECP and sIL5Ralpha were significantly elevated in AE-COPD subjects (n = 54) compared to healthy controls (n = 11, p = 0.018). Furthermore, there was a significant increase in sIL5Ralpha, but not in ECP, in 30 patients with virus-associated AE-COPD compared to smokers without COPD (n = 16) and healthy controls. The increase in FEV(1) after resolution of the AE-COPD correlated with the decrease in sIL5Ralpha (r = 0.269, p = 0.034). CONCLUSIONS: sIL5Ralpha is increased in AE-COPD and not affected by smoking like ECP. sIL5Ralpha is increased in patients with virus-associated AE-COPD compared to smokers and controls. Concentrations of sIL5Ralpha mirror changes in the clinical status and lung function. These data support the involvement of eosinophils in acute exacerbations of COPD.     

沙美特罗/氟替卡松对COPD患者炎症介质的影响

目的:观察吸入沙美特罗/氟替卡松干粉对稳定期中重度慢性阻塞性肺疾病(COPD)患者气道炎症的影响.方法:60例患者随机分为治疗组28例和对照组32例,对照组按需吸入沙丁胺醇气雾剂,治疗组吸入沙美特罗/氟替卡松干粉剂治疗.观察两组治疗前后血清及诱导痰炎症介质(IL-8、TNF-α)的变化.结果:治疗3个月后血清及诱导痰中...     

Eotaxin in induced sputum of asthmatics: relationship with eosinophils and eosinophil cationic protein in sputum

BACKGROUND: Eosinophilic inflammation is a crucial aspect of allergic diseases such as bronchial asthma. An eosinophil-active chemokine, eotaxin, may play a role in the pathogenesis of the tissue eosinophilia accompanying asthma. METHODS: Induced sputa were obtained from 53 patients with atopic asthma and six healthy subjects, and the concentration of eotaxin in the sputum was measured by ELISA. We investigated whether the sputum content of eotaxin is related to 1) asthma status or corticosteroid therapy, and 2) other sputum indices, including percentage of eosinophils and concentration of eosinophil cationic protein (ECP). RESULTS: The patients with stable or unstable asthma showed significantly higher concentrations of sputum eotaxin than the normal controls. The level of sputum eotaxin demonstrated a positive correlation with the percentage of eosinophils in stable asthmatics not receiving corticosteroid therapy, but not in stable patients treated with corticosteroids, or in unstable patients. Sputum eotaxin demonstrated a positive correlation with ECP in asthmatic patients who were either in a stable state or not receiving steroid therapy. CONCLUSIONS: The elevated level of eotaxin detected in association with increased eosinophils and ECP in the sputum of asthmatics suggests that eotaxin is involved in the pathogenesis of eosinophilic airway inflammation. The relationship of eotaxin to airway eosinophilia may be modified by the stability status of asthma and corticosteroid therapy.     

Airway inflammation in asthma and perennial allergic rhinitis. Relationship with nonspecific bronchial responsiveness and maximal airway narrowing

BACKGROUND: Eosinophilic airway inflammation is the hallmark of asthma, but it has also been reported in other conditions such as allergic rhinitis. We have tested whether the analysis of cells and chemicals in sputum can distinguish between patients with mild allergic asthma, those with allergic rhinitis, and healthy controls. The relationship between inflammation markers in sputum and nonspecific bronchial hyperresponsiveness to methacholine (BHR) (PD20 and maximal response plateau [MRP] values) was also evaluated. METHODS: We selected 31 mild asthmatics and 15 rhinitis patients sensitized to house-dust mite. As a control group, we studied 10 healthy subjects. Every subject underwent the methacholine bronchial provocation test (M-BPT) and sputum induction. Blood eosinophils and serum ECP levels were measured. Sputum cell differentials were assessed, and eosinophil cationic protein (ECP), tryptase, albumin, and interleukin (IL)-5 levels were measured in the entire sputum supernatant. RESULTS: Blood eosinophils and serum ECP levels were higher in asthma patients and rhinitis than in healthy controls, but no difference between asthma patients and rhinitis patients was found. Asthmatics had higher eosinophil counts and higher ECP and tryptase levels in sputum than rhinitis patients or control subjects. Sputum albumin levels were higher in asthmatics than in controls. Rhinitis patients exhibited higher sputum eosinophils than healthy controls. An association between sputum eosinophil numbers and MPR values (r= -0.57) was detected, and a trend toward correlation between sputum ECP levels and PD20 values (r= -0.47) was found in the rhinitis group, but not in asthmatics. No correlation between blood eosinophilic inflammation and lung functional indices was found. CONCLUSIONS: Induced sputum is an accurate method to study bronchial inflammation, allowing one to distinguish between rhinitis patients and mildly asthmatic patients. The fact that no relationship was detected between sputum inflammation and BHR suggests that other factors, such as airway remodeling, may be at least partly responsible for BHR in asthma.     

The small airway inflammation of asthmatic patients who have used dry powder type inhaled steroid for moderate-long term evaluated by induced sputum and the efficacy of HFA-BDP (QVAR) inhalation]

Although the dry powder type inhaled steroids, such as Fluticasone Propionate Diskhaler (FP-DH), FP Diskus (FP-DK), Budesonide Turbuhaler (BUD-TH), are widely distributed in daily clinical fields, we clinicians are required to evaluate whether it is effectively inhibiting inflammation of distal airway or not. We also investigated the effect of Hydrofluoroalukan-beclomethasone dipropionate (HFA-BDP), a new type of inhaled steroid which forms super micro aerosol particles, in the distal small airway. METHOD: 85 patients with moderate asthma, who daily used dry powder type inhaled steroid for at least more than 6 months with stable asthmatic condition, were the subject of this study. All subjects underwent sputum induction with the inhalation of 10% of hypertonic saline solution for 15 min and eosinophil counts and eosinophil cationic protein (ECP) in individual induced sputum were measured. Then, patients who had eosinophils detected in their induced sputum changed their previously inhaled steroid to HFA-BDP inhalation (400 i.g./day). Their eosinophil counts and the values of eosinophil cationic protein (ECP), Eotaxin, RANTES and neutrophil elastase (PMN-E) in their induced sputum were also examined before and 4weeks after changing HFA-BDP inhalation. RESULT: Increased eosinophils were found in the induced sputum of 40.5% patients of the FP-DK group, 36.3% of the FP-DH group and 32.4% of the BUD-TH group, respectively. Compared with group of patients in which no sputum eosinophil were detected, the sputum ECP values, in which sputum eosinophils were detected, were significantly high. 4 weeks after changing to HFA-BDP inhalation, eosinophil counts, ECP, Eotaxin, RANTES and PMN-E in their induced sputum were decreased in every group. CONCLUSION: Compared with the ordinary dry powder type inhaled steroids, HFA-BDP can effectively diminish distal airway inflammation, suggesting the possibility that HFA-BDP can effectively reach to the distal small airway by forming super micro aerosol particles.     

Accuracy of eosinophils and eosinophil cationic protein to predict steroid improvement in asthma

BACKGROUND: There is a large variability in clinical response to corticosteroid treatment in patients with asthma. Several markers of inflammation like eosinophils and eosinophil cationic protein (ECP), as well as exhaled nitric oxide (NO), are good candidates to predict clinical response. AIM: We wanted to determine whether we could actually predict a favourable response to inhaled corticosteroids in individual patients. METHODS: One hundred and twenty patients with unstable asthma were treated with either prednisolone 30 mg/day, fluticasone propionate 1000 microg/day b.i.d. or fluticasone propionate 250 microg/day b.i.d., both via Diskhaler. They were treated during 2 weeks, in a double-blind, parallel group, double dummy design. We measured eosinophils and ECP in blood and sputum, and exhaled nitric oxide as inflammatory parameters before and after 2 weeks in order to predict the changes in forced expiratory volume in 1 s (FEV1), provocative concentration of methacholine causing a 20% fall in FEV1 (PC20 Mch), and asthma quality of life (QOL). Secondly, to test whether these results were applicable in clinical practice we determined the individual prediction of corticosteroid response. RESULTS: We found that changes in FEV1, PC20 Mch and QOL with corticosteroids were predominantly predicted by their respective baseline value and to a smaller extent by eosinophils in blood or sputum. ECP, measured in blood or sputum, was certainly not better than eosinophils in predicting clinical response to corticosteroids. Smoking status was an additional predictor for change in FEV1, but not for change in PC20 Mch or QOL. Prediction of a good clinical response was poor. For instance, high sputum eosinophils (> or = 3%) correctly predicted an improvement in PC20 Mch in only 65% of the patients. CONCLUSION: Our findings show that baseline values of the clinical parameters used as outcome parameters are the major predictors of clinical response to corticosteroids. Eosinophil percentage in blood or sputum adds to this, whereas ECP provides no additional information. Correct prediction of clinical response in an individual patient, however, remains poor with our currently used clinical and inflammatory parameters.     

Can hypertonic saline inhalation influence preformed chemokine and mediator release in induced sputum of chronic obstructive pulmonary disease patients? Comparison with isotonic saline

Background Hypertonic saline (HS) has been shown to modulate in vitro cell functions according to the state of cell activation; however, few studies have evaluated the effect of HS in vivo. Chronic airway inflammation, a major feature of chronic obstructive pulmonary disease (COPD), is associated with an activation of inflammatory and resident cells, which in turn makes them more prompt to respond to further stimuli. Objective To evaluate whether HS might modulate, also in vivo, the release of preformed mediators and intracellular chemokines from airway cells of COPD patients. Methods Sputum was induced by inhalation of either HS (4.5% w/v) or isotonic saline (IS 0.9% w/v) solution and processed by plug selection. We measured eosinophil cationic protein (ECP), neutrophil elastase (NE), IL‐8 and monocyte chemoattractant protein‐1 (MCP‐1) in sputum samples obtained by either HS or IS inhalation in 24 COPD patients. Results No significant difference in mediators measured in sputum samples obtained by the two different inductions was observed; also, there was no significant difference in sputum sample volumes, cell viability, total and differential cell counts. Repeatability between the two tests was high for ECP, NE, macrophages, neutrophils and eosinophils, and satisfactory for IL‐8 and MCP‐1. Conclusions Hyperosmolarity does not affect the levels of the inflammatory mediators and chemokines examined or the cell counts measured in induced sputum obtained from COPD patients. This study does not support the hypothesis that HS can stimulate chemokine and mediator release from airway cells of COPD patients. Therefore, HS and IS can be interchangeably used to measure inflammatory mediators in the sputum supernatant of COPD patients.     

Relationship between sputum inflammatory markers and osmotic airway hyperresponsiveness during induction of sputum in asthmatic patients

Hypertonic saline aerosols are being used increasingly for bronchial provocation testing and induction of sputum. The aims of this study were to assess the response to challenge with 3% hypertonic saline administered via a ultrasonic nebulizer in patients with asthma, and to evaluate relationship between % fall of FEV1 during induction of sputum (osmotic airway hyperresponsiveness; osmotic AHR) and biochemical markers of induced sputum. We investigated changes in FEV1 in response to inhaling ultrasonically nebulized 3% saline in 25 patients with asthma and 10 control subjects. FEV1 was measured before, during, and after induction of sputum. We used fluoroimmunoassay to detect eosinophil cationic protein (ECP), immunohistochemical staining to detect EG2+ (secretory form of ECP) eosinophils, and a sandwich ELISA to detect interleukin (IL)-5. Protein concentration was determined by using bicinchoninic acid protein assay reagent. Asthmatics, compared with controls, had significantly higher osmotic AHR. Moderate to severe asthmatics had significantly higher osmotic AHR compared to mild asthmatics. Osmotic AHR was significantly correlated with the proportion of eosinophils, the levels of ECP, EG2+ eosinophils, IL-5, and proteins. These data suggest that osmotic AHR is closely related to the clinical status and biochemical markers of sputum supernatant in asthmatic patients.     

Eosinophils and eosinophilic cationic protein in induced sputum and blood: effects of budesonide and terbutaline treatment.

BACKGROUND: There is a need for easily measurable markers of airway inflammation to guide the use of anti-inflammatory treatment in asthma. Eosinophilic cationic protein (ECP) levels in sputum and blood correlate with clinical severity, and serial measurements of ECP have been proposed as a suitable candidate. AIMS AND METHODS: Our aim was to confirm that sputum and serum ECP measurements would provide a more sensitive indicator of responses to asthma treatment than eosinophil counts per se, in a randomized, placebo-controlled, crossover study of terbutaline, budesonide, and their combination in patients with chronic persistent asthma. We compared the changes in eosinophil counts and ECP in induced sputum and blood during each treatment period. RESULTS: Budesonide and combined treatment caused a significant reduction in sputum eosinophils (-2.7% and -2.3%, respectively, P < 0.05). Sputum eosinophils increased with terbutaline (+3.9%, P = 0.049). In contrast, the changes for sputum ECP were not significant. There was a similar treatment effect on blood eosinophils, but not for serum ECP. Correlations between sputum and blood eosinophils were significant with and without budesonide, but were nonsignificant between sputum and blood ECP during the active treatments. Correlations between sputum eosinophils and ECP, and between blood eosinophils and serum ECP were greatest during treatment with placebo or terbutaline alone: budesonide weakened or abolished these relationships. CONCLUSIONS: Compared with eosinophil counts, ECP measurements in either induced sputum or serum failed to reflect treatment-related changes in chronic asthma. We conclude that ECP is not a sensitive or reliable means of evaluating airway inflammation, and can not be recommended for assessing responses to anti-inflammatory therapy.