Neutrophil Extracellular Traps Identification in Tegumentary Lesions of Patients with Paracoccidioidomycosis and Different Patterns of NETs Generation In Vitro

Paracoccidioidomycosis (PCM) is a systemic mycosis, endemic in most Latin American countries, especially in Brazil. It is caused by the thermo-dimorphic fungus of the genus Paracoccidioides (Paracoccidioides brasiliensis and Paracoccidioides lutzii). Innate immune response plays a crucial role in host defense against fungal infections, and neutrophils (PMNs) are able to combat microorganisms with three different mechanisms: phagocytosis, secretion of granular proteins, which have antimicrobial properties, and the most recent described mechanism called NETosis. This new process is characterized by the release of net-like structures called Neutrophil Extracellular Traps (NETs), which is composed of nuclear (decondensed DNA and histones) and granular material such as elastase. Several microorganisms have the ability of inducing NETs formation, including gram-positive and gram-negative bacteria, viruses and some fungi. We proposed to identify NETs in tegumentary lesions of patients with PCM and to analyze the interaction between two strains of P. brasiliensis and human PMNs by NETs formation in vitro. In this context, the presence of NETs in vivo was evidenced in tegumentary lesions of patients with PCM by confocal spectrum analyzer. Furthermore, we showed that the high virulent P. brasiliensis strain 18 (Pb18) and the lower virulent strain Pb265 are able to induce different patterns of NETs formation in vitro. The quantification of extracellular DNA corroborates the idea of the ability of P. brasiliensis in inducing NETs release. In conclusion, our data show for the first time the identification of NETs in lesions of patients with PCM and demonstrate distinct patterns of NETs in cultures challenged with fungi in vitro. The presence of NETs components both in vivo and in vitro open new possibilities for the detailed investigation of immunity in PCM.     

Cytokines Induced Neutrophil Extracellular Traps Formation: Implication for the Inflammatory Disease Condition

Neutrophils (PMNs) and cytokines have a critical role to play in host defense and systemic inflammatory response syndrome (SIRS). Neutrophil extracellular traps (NETs) have been shown to extracellularly kill pathogens, and inflammatory potential of NETs has been shown. Microbial killing inside the phagosomes or by NETs is mediated by reactive oxygen and nitrogen species (ROS/RNS). The present study was undertaken to assess circulating NETs contents and frequency of NETs generation by isolated PMNs from SIRS patients. These patients displayed significant augmentation in the circulating myeloperoxidase (MPO) activity and DNA content, while PMA stimulated PMNs from these patients, generated more free radicals and NETs. Plasma obtained from SIRS patients, if added to the PMNs isolated from healthy subjects, enhanced NETs release and free radical formation. Expressions of inflammatory cytokines (IL-1β, TNFα and IL-8) in the PMNs as well as their circulating levels were significantly augmented in SIRS subjects. Treatment of neutrophils from healthy subjects with TNFα, IL-1β, or IL-8 enhanced free radicals generation and NETs formation, which was mediated through the activation of NADPH oxidase and MPO. Pre-incubation of plasma from SIRS with TNFα, IL-1β, or IL-8 antibodies reduced the NETs release. Role of IL-1β, TNFα and IL-8 thus seems to be involved in the enhanced release of NETs in SIRS subjects.     

Systemic and Pulmonary Vascular Remodelling in Chronic Obstructive Pulmonary Disease

BackgroundChronic Obstructive Pulmonary Disease (COPD) is associated with subclinical systemic atherosclerosis and pulmonary vascular remodelling characterized by intimal hyperplasia and luminal narrowing. We aimed to determine differences in the intimal thickening of systemic and pulmonary arteries in COPD subjects and smokers. Secondary aims include comparisons with a non-smokers group; determining the clinical variables associated with systemic and pulmonary intimal thickening, and the correlations between systemic and pulmonary remodelling changes.MethodsAll consecutive subjects undergoing lung resection were included and divided into 3 groups: 1) COPD, 2) smokers, and 3) non-smokers. Sections of the 5th intercostal artery and muscular pulmonary arteries were measured by histo-morphometry. Four parameters of intimal thickening were evaluated: 1) percentage of intimal area (%IA), 2) percentage of luminal narrowing, 3) intimal thickness index, and 4) intima-to-media ratio.ResultsIn the adjusted analysis, the systemic arteries of COPD subjects showed greater intimal thickening (%IA) than those of smokers (15.6±1.5% vs. 14.2±1.6%, p = 0.038). In the pulmonary arteries, significant differences were observed for %IA between the 2 groups (37.3±2.2% vs. 29.3±2.3%, p = 0.016). Among clinical factors, metabolic syndrome, gender and COPD status were associated with the systemic intimal thickening, while only COPD status was associated with pulmonary intimal thickening. A correlation between the %IA of the systemic and pulmonary arteries was observed (Spearman’s rho = 0.46, p = 0.008).ConclusionsGreater intimal thickening in systemic and pulmonary arteries is observed in COPD patients than in smokers. There is a correlation between systemic and pulmonary vascular remodelling in the overall population.     

Prevalence and Global Initiative for Chronic Obstructive Lung Disease Group Distribution of Chronic Obstructive Pulmonary Disease Detected by Preoperative Pulmonary Function Test

Background

Despite being a major public health problem, chronic obstructive pulmonary disease (COPD) remains underdiagnosed, and only 2.4% COPD patients are aware of their disease in Korea. The objective of this study was to estimate the prevalence of COPD detected by spirometry performed as a preoperative screening test and to determine the Global Initiative for Chronic Obstructive Lung Disease (GOLD) group distribution and self-awareness of COPD.

Methods

We reviewed the medical records of adults (age, ≥40 years) who had undergone spirometry during preoperative screening between April and August 2013 at a tertiary hospital in Korea. COPD was defined as a postbronchodilator forced expiratory volume in 1 s/forced vital capacity ratio of <0.7. We analyzed self-administered COPD questionnaires for the assessment of the frequency of acute exacerbation over the previous year and dyspnea severity using the modified Medical Research Council dyspnea scale and COPD assessment test.

Results

Among 3029 patients aged >40 years who had undergone spirometry as a preoperative screening test, 474 (15.6%; 404 men; median age, 70 years; range, 44–93 years) were diagnosed with COPD. Only 26 (5.5%) patients reported previous diagnosis of COPD (2.1%), emphysema (0.8%), or chronic bronchitis (2.5%). The GOLD group distribution was as follows: 63.3% in group A, 31.2% in group B, 1.7% in group C, and 3.8% in group D.

Conclusions

The prevalence of COPD diagnosed by preoperative spirometry was 15.6%, and only 5.5% patients were aware of their disease. Approximately one-third of the COPD patients belonged to GOLD groups B, C, and D, which require regular treatment.     

慢性阻塞性肺病大鼠模型的建立和比较评估

目的:动态观察运用不同方法建立的两种实验性大鼠慢性阻塞性肺疾病(COPD)模型并比较评估两组模型的特点.方法:分别采用单纯被动吸烟(单一组)和被动吸烟与细菌内毒素(LPS)气管注入的复合方法(复合组)制造大鼠COPD模型,运用HE染色及半定量图像分析法对比研究两组模型肺组织及小支气管的病理形态学改变.结果:建立的COPD大鼠模型均符合人类COPD的病理形态学特点;复合组的气道慢性炎症、重塑改变及气流阻塞情况均较单一组严重;单一组、复合组模型各时间段管壁及平滑肌层均较正常对照组显著增厚(P＜0.01),第20天时复合组管壁及平滑肌层均较单一组显著增厚(P＜0.01),而第40天及60天时复合组仅管壁较单一组显著增厚(P＜0.01).结论:COPD模型的形成是由于慢性气道炎症的反复刺激引起管壁纤维性增生增厚及平滑肌层增厚,即气道重塑,最终导致气流受限;复合组COPD模型的气道炎症及气道重塑均较单一组COPD模型显著.     

多层螺旋CT测定肺容积指标对慢性阻塞性肺疾病的诊断价值探讨

目的：分析多层螺旋CT检测慢性阻塞性肺疾病患者肺容积指数的准确性,探讨多层螺旋CT的诊断价值,为慢性阻塞性肺病的临床诊断提供可借鉴的方法。方法：选取2010年10月-2012年8月我院收治的慢性阻塞性肺疾病患者98例为观察组,另选取同期接受体检的健康志愿者70例为对照组。采用多层螺旋CT测定两组不同肺区的肺容积指标并与临床PFT指标进行相关性分析。结果：对照组与观察组的肺功能指标存在显著差异（P〈0.05）;观察组患者在不同肺区测定的Vin及上肺区Vin-Vex值无统计学意义（P〉0.05）;最大呼气末容积（Vex）、容积比（Vex/Vin）和肺容积变化比率[（Vin-Vex）/Vin]均呈显著差异,具有统计学意义（P〈0.05）;肺容积差（Vin-Vex）与各项PFT指标无相关性（P〉0.05）。结论：64层螺旋CT肺容积成像对诊断COPD有预测意义,值得临床上进一步研究和推广。     

Vibrio cholerae Evades Neutrophil Extracellular Traps by the Activity of Two Extracellular Nucleases

The Gram negative bacterium Vibrio cholerae is the causative agent of the secretory diarrheal disease cholera, which has traditionally been classified as a noninflammatory disease. However, several recent reports suggest that a V. cholerae infection induces an inflammatory response in the gastrointestinal tract indicated by recruitment of innate immune cells and increase of inflammatory cytokines. In this study, we describe a colonization defect of a double extracellular nuclease V. cholerae mutant in immunocompetent mice, which is not evident in neutropenic mice. Intrigued by this observation, we investigated the impact of neutrophils, as a central part of the innate immune system, on the pathogen V. cholerae in more detail. Our results demonstrate that V. cholerae induces formation of neutrophil extracellular traps (NETs) upon contact with neutrophils, while V. cholerae in return induces the two extracellular nucleases upon presence of NETs. We show that the V. cholerae wild type rapidly degrades the DNA component of the NETs by the combined activity of the two extracellular nucleases Dns and Xds. In contrast, NETs exhibit prolonged stability in presence of the double nuclease mutant. Finally, we demonstrate that Dns and Xds mediate evasion of V. cholerae from NETs and lower the susceptibility for extracellular killing in the presence of NETs. This report provides a first comprehensive characterization of the interplay between neutrophils and V. cholerae along with new evidence that the innate immune response impacts the colonization of V. cholerae in vivo. A limitation of this study is an inability for technical and physiological reasons to visualize intact NETs in the intestinal lumen of infected mice, but we can hypothesize that extracellular nuclease production by V. cholerae may enhance survival fitness of the pathogen through NET degradation.     

Effects of N-Acetylcysteine in Ozone-Induced Chronic Obstructive Pulmonary Disease Model

Introduction

Chronic exposure to high levels of ozone induces emphysema and chronic inflammation in mice. We determined the recovery from ozone-induced injury and whether an antioxidant, N-acetylcysteine (NAC), could prevent or reverse the lung damage.

Methods

Mice were exposed to ozone (2.5 ppm, 3 hours/12 exposures, over 6 weeks) and studied 24 hours (24h) or 6 weeks (6W) later. Nac (100 mg/kg, intraperitoneally) was administered either before each exposure (preventive) or after completion of exposure (therapeutic) for 6 weeks.

Results

After ozone exposure, there was an increase in functional residual capacity, total lung volume, and lung compliance, and a reduction in the ratio of forced expiratory volume at 25 and 50 milliseconds to forced vital capacity (FEV₂₅/FVC, FEV₅₀/FVC). Mean linear intercept (L_m) and airway hyperresponsiveness (AHR) to acetylcholine increased, and remained unchanged at 6W after cessation of exposure. Preventive NAC reduced the number of BAL macrophages and airway smooth muscle (ASM) mass. Therapeutic NAC reversed AHR, and reduced ASM mass and apoptotic cells.

Conclusion

Emphysema and lung function changes were irreversible up to 6W after cessation of ozone exposure, and were not reversed by NAC. The beneficial effects of therapeutic NAC may be restricted to the ASM.     

Circulating Progenitor Cells and Vascular Dysfunction in Chronic Obstructive Pulmonary Disease

Background

In chronic obstructive pulmonary disease (COPD), decreased progenitor cells and impairment of systemic vascular function have been suggested to confer higher cardiovascular risk. The origin of these changes and their relationship with alterations in the pulmonary circulation are unknown.

Objectives

To investigate whether changes in the number of circulating hematopoietic progenitor cells are associated with pulmonary hypertension or changes in endothelial function.

Methods

62 COPD patients and 35 controls (18 non-smokers and 17 smokers) without cardiovascular risk factors other than cigarette smoking were studied. The number of circulating progenitors was measured as CD45⁺CD34⁺CD133⁺ labeled cells by flow cytometry. Endothelial function was assessed by flow-mediated dilation. Markers of inflammation and angiogenesis were also measured in all subjects.

Results

Compared with controls, the number of circulating progenitor cells was reduced in COPD patients. Progenitor cells did not differ between control smokers and non-smokers. COPD patients with pulmonary hypertension showed greater number of progenitor cells than those without pulmonary hypertension. Systemic endothelial function was worse in both control smokers and COPD patients. Interleukin-6, fibrinogen, high sensitivity C-reactive protein, vascular endothelial growth factor and tumor necrosis factor were increased in COPD. In COPD patients, the number of circulating progenitor cells was inversely related to the flow-mediated dilation of systemic arteries.

Conclusions

Pulmonary and systemic vascular impairment in COPD is associated with cigarette smoking but not with the reduced number of circulating hematopoietic progenitors. The latter appears to be a consequence of the disease itself not related to smoking habit.     

老年慢性阻塞性肺疾病与继发性骨质疏松症的相关性分析

目的:分析老年慢性阻塞性肺疾病与继发性骨质疏松症的相关性.方法:选择我院收治的54例老年慢性阻塞性肺疾病患者为实验组及38例同期在我院治疗的肺功能正常的非COPD患者为对照组,分析和比较其腰椎(L1-4)和股骨近端的骨密度、肺功能、血气以及血钙、磷等生化指标.结果:实验组腰椎(L1-4)和股骨近端的骨密度均显著低于对照组.不同严重程度的COPD患者骨质疏松的发生率均显著高于对照组,且随着COPD患者病情严重程度的增加,骨质疏松的发生率逐渐上升.实验组骨密度的降低与PaO2的变化呈显著正相关.结论:老年慢性阻塞性肺疾病患者易发生骨质疏松,低氧血症可能是其并发骨质疏松的重要危险因素之一.     

Indacaterol for Chronic Obstructive Pulmonary Disease: Systematic Review and Meta-Analysis

Background

Inhaled bronchodilators are the first-line therapy for COPD. Indacaterol is a novel addition to existing long-acting bronchodilators.

Objectives

Systematic review of randomized controlled trials (RCT) on efficacy and safety of indacaterol as compared: 1) with placebo at different dosages, 2) with existing bronchodilators; (3) as add-on treatment to tiotropium.

Methods

We searched 13 electronic databases, including MEDLINE, EMBASE and CENTRAL, and contacted the manufacturer for unpublished data. Primary outcome was mean FEV1 change at 12^th week, secondary outcomes included changes in SGRQ, TDI and BODE index at 6 months, exacerbation at 1 year, and worsening of symptoms.

Results

Twelve eligible RCTs of moderate risk of bias included data from 10,977 patients. Compared to placebo, indacaterol improved FEV1 by a weighted mean difference (WMD) of 0.16 L (95%CI: 0.15, 0.18 L, p<0.001), homogeneously above the minimally important difference of 0.10 L. It offered clinically relevant improvement in all secondary outcomes except exacerbation. Magnitude of benefit did not differ significantly by dosage, but one treatment related death was reported at 300 ug. Efficacy of Indacaterol was similar to formoterol and salmeterol (FEV1 WMD = 0.04L, 95%CI: 0.01L, 0.07 L, p = 0.02); and tiotropium (FEV1 WMD = 0.01L, 95%CI: −0.01, 0.03L, p = 0.61). The use of indacaterol on top of tiotropium yielded additional improvement on FEV1 (WMD = 0.07 L, 95%CI: 0.05L, 0.10 L, p<0.001).

Conclusion

Indacaterol is safe and beneficial for patients with COPD at dosage ≤150 ug. It may serve as a good alternative to existing bronchodilators, or as an add-on to tiotropium for unresponsive patients. Use of higher dosage requires further justification.     

慢性阻塞性肺疾病发病机制的研究进展

慢性阻塞性肺疾病(chronic obstructive pulmonary disease, COPD)是呼吸系统中的常见病和多发病,其发病率和致死率居高不下。根据WHO调查数据显示,预计到2020年, COPD将成为全球第三大致死病因。COPD的形成与发展涉及众多因素,包括遗传因素和环境因素等。COPD的发病机制至今未明,氧化应激、炎症机制、蛋白酶/抗蛋白酶失衡以及细胞凋亡与之密切相关。另外,自身免疫反应、微生物组的变化以及无效的受损修复在COPD的发病机制中同样具有关键作用。因此,深入了解并研究COPD的发病机制对预防与治疗该疾病具有重要意义。     

情绪调节自我效能感对慢性阻塞性肺疾病患者治疗的影响

目的:本研究探讨心理干预对患者情绪调节自我效能感的影响,分析情绪调节自我效能感对慢性阻塞性肺疾病患者治疗和康复的影响.方法:1)实验分为干预组(实验组)和非干预组(对照).2)情绪调节自我效能感量表评定患者干预前后的情绪调节自我效能感.3)对心理干预组进行随访,使用理性情绪化疗法、支持疗法、情绪宣泄法、康复指导及疾病意外应对指导进行干预.结果:1)为其1年心理干预有效降低疾病复发率、住院时间和住院频率.但对急性发作治疗期的治疗影响不显著.2)心理干预有效提高患者的情绪调节自我效能感.结论:心理干预有效提高患者的情绪调节自我效能感,促进缓解期的慢性阻塞性肺疾病患者的康复,并有效降低复发率.     

慢性阻塞性肺病动物模型的研究进展

慢性阻塞性肺病(COPD)是一种严重的呼吸系统疾病,该病主要包括慢性肺气肿及慢性支气管炎,其发病率、死亡率高,医疗负担重。由于其发病机制、临床发展过程较为复杂,对COPD诊断、治疗的研究工作进展仍然相当缓慢。目前,国内外研究人员通过建立COPD动物模型对该病进行了大量研究工作。旨在对COPD动物模型的建立及评价方法进行总结,并对模型动物选择,评价方法的选择提出一点新的思路。     

In Vivo Characterization of Neutrophil Extracellular Traps in Various Organs of a Murine Sepsis Model

Neutrophil extracellular traps (NETs) represent extracellular microbial trapping and killing. Recently, it has been implicated in thrombogenesis, autoimmune disease, and cancer progression. The aim of this study was to characterize NETs in various organs of a murine sepsis model in vivo and to investigate their associations with platelets, leukocytes, or vascular endothelium. NETs were classified as two distinct forms; cell-free NETs that were released away from neutrophils and anchored NETs that were anchored to neutrophils. Circulating cell-free NETs were characterized as fragmented or cotton-like structures, while anchored NETs were characterized as linear, reticular, membranous, or spot-like structures. In septic mice, both anchored and cell-free NETs were significantly increased in postcapillary venules of the cecum and hepatic sinusoids with increased leukocyte-endothelial interactions. NETs were also observed in both alveolar space and pulmonary capillaries of the lung. The interactions of NETs with platelet aggregates, leukocyte-platelet aggregates or vascular endothelium of arterioles and venules were observed in the microcirculation of septic mice. Microvessel occlusions which may be caused by platelet aggregates or leukocyte-platelet aggregates and heterogeneously decreased blood flow were also observed in septic mice. NETs appeared to be associated with the formation of platelet aggregates or leukocyte-platelet aggregates. These observational findings may suggest the adverse effect of intravascular NETs on the host during a sepsis.     

Periodontal Disease and Risk of Chronic Obstructive Pulmonary Disease: A Meta-Analysis of Observational Studies

Background

Many epidemiological studies have found a positive association between periodontal disease (PD) and risk of chronic obstructive pulmonary disease (COPD), but this association is varied and even contradictory among studies. We performed a meta-analysis to ascertain the relationship between PD and COPD.

Methods

PubMed and Embase database were searched up to January 10, 2012, for relevant observational studies on the association between PD and risk of COPD. Data from the studies selected were extracted and analyzed independently by two authors. The meta-analysis was performed using the Comprehensive Meta-Analysis software.

Results

Fourteen observational studies (one nested case-control, eight case-control, and five cross-sectional) involving 3,988 COPD patients were yielded. Based on random-effects meta-analysis, a significant association between PD and COPD was identified (odds ratio = 2.08, 95% confidence interval = 1.48–2.91; P<0.001), with sensitivity analysis showing that the result was robust. Subgroups analyses according to study design, ethnicity, assessment of PD/COPD, and adjusted/unadjusted odds ratios also revealed a significant association. Publication bias was detected.

Conclusions

Based on current evidence, PD is a significant and independent risk factor of COPD. However, whether a causal relationships exists remains unclear. Morever, we suggest performing randomized controlled trails to explore whether periodontal interventions are beneficial in regulating COPD pathogenesis and progression.     

Predictors of Exacerbations in Chronic Obstructive Pulmonary Disease - Results from the Bergen COPD Cohort Study

Background

COPD exacerbations accelerate disease progression.

Aims

To examine if COPD characteristics and systemic inflammatory markers predict the risk for acute COPD exacerbation (AECOPD) frequency and duration.

Methods

403 COPD patients, GOLD stage II-IV, aged 44–76 years were included in the Bergen COPD Cohort Study in 2006/07, and followed for 3 years. Examined baseline predictors were sex, age, body composition, smoking, AECOPD the last year, GOLD stage, Charlson comorbidity score (CCS), hypoxemia (PaO2<8 kPa), cough, use of inhaled steroids, and the inflammatory markers leucocytes, C-reactive protein (CRP), neutrophil gelatinase associated lipocalin (NGAL), soluble tumor necrosis factor receptor 1 (sTNF-R1), and osteoprotegrin (OPG). Negative binomial models with random effects were fitted to estimate the annual incidence rate ratios (IRR). For analysis of AECOPD duration, a generalized estimation equation logistic regression model was fitted, also adjusting for season, time since inclusion and AECOPD severity.

Results

After multivariate adjustment, significant predictors of AECOPD were: female sex [IRR 1.45 (1.14–1.84)], age per 10 year increase [1.23 (1.03–1.47)], >1 AECOPD last year before baseline [1.65 (1.24–2.21)], GOLD III [1.36 (1.07–1.74)], GOLD IV [2.90 (1.98–4.25)], chronic cough [1.64 (1.30–2.06)] and use of inhaled steroids [1.57 (1.21–2.05)]. For AECOPD duration more than three weeks, significant predictors after adjustment were: hypoxemia [0.60 (0.39–0.92)], years since inclusion [1.19 (1.03–1.37)], AECOPD severity; moderate [OR 1.58 (1.14–2.18)] and severe [2.34 (1.58–3.49)], season; winter [1.51 (1.08–2.12)], spring [1.45 (1.02–2.05)] and sTNF-R1 per SD increase [1.16 (1.00–1.35)].

Conclusion

Several COPD characteristics were independent predictors of both AECOPD frequency and duration.     

不同气候条件下慢性阻塞性肺疾病的病原学和免疫学研究

目的：探讨COPD患者不同气候条件下（雷暴、阴雨、台风）的病原学和免疫功能。方法：细菌鉴定采用VITEK全自动微生物鉴定系统。K．B纸片扩散法测定药敏。T淋巴细胞亚群测定采用单克隆抗体免疫组化荧光染色法。血清免疫球蛋白（IgG,IgA,IgM）用琼脂单向扩散法。结果：台风、雷暴、阴雨、天气气候条件60例患者痰培养阳性率分别为45％、40％、30％,占革兰阴性菌前2位分别为肺炎克雷伯杆菌、流感嗜血杆菌和肺炎克雷伯杆菌、大肠埃希杆菌及流感嗜血杆菌、铜绿假单胞菌。革兰阳性菌中分别以肺炎链球菌、金黄色葡萄球菌为主及肺炎链球菌、金黄色葡萄球菌为主和金黄色葡萄球菌、表皮葡萄球菌为主。铜绿假单胞菌、肺炎克雷伯杆菌、流感嗜血杆菌对常用抗生素具有较高的耐药性。台风、雷暴、阴雨气候条件下3组AECOPD患者CD3＋ CD4＋、CD4＋／CD8＋、IgG、IgA、IgM均明显低于健康对照组（P〈0．05）,CD8＋高于健康对照组（P〈0．05）,而发作期和缓解期无显著差异（P〉0．05）。三种气候条件下相互之间比较的细胞和体液免疫指标比较无显著差剐（P〉0．05）。结论：雷暴、阴雨、台风条件下AECOPD的患者存在病原学分布差异,对常用抗生素具有较高的耐药性,细胞和体液免疫功能进一步下降。但三者相互之间的免疫功能比较无明显差异。     

顺尔宁对稳定期慢性阻塞性肺疾病患者的疗效分析

目的：探讨顺尔宁治疗稳定期慢性阻塞性肺疾病（COPD）患者的临床效果。方法：将60例稳定期COPD患者随机分为研究组和对照组,每组各30例。经2周洗脱期后,对照组采用常规治疗,研究组在常规治疗基础上加用顺尔宁治疗,共治疗4周。比较两组患者肺功能参数、血气分析、生活质量以及血清LTB4、IL-8浓度的变化。结果：治疗后两组患者的肺功能参数、血气分析指标和生活质量均有改善,研究组肺功能参数改善程度较对照组显著（P〈0．05）;研究组的生活质量改善明显优于对照组（P〈0．05）：治疗后两组患者的血清LTB4、IL-8水平较治疗前均下降,且研究组明显低于对照组（P〈0．05）。结论：顺尔宁能降低稳定期慢性阻塞性肺疾病患者血清LTB4、IL-8含量,改善患者肺功能及血气分析指标,有效提高患者的生命质量,值得临床推广。