慢性阻塞性肺疾病病人外周血T淋巴细胞的检测及意义

目的检测慢性阻塞性肺疾病(COPD)患者体内各类T淋巴细胞的亚群,了解COPD患者的细胞免疫功能状态。方法采用免疫荧光双标记法和流式细胞仪检测COPD患者外周血中的T淋巴细胞及其亚群。结果与健康对照组相比较,急性期COPD组患者CD3+T细胞及CD4+T细胞亚群下降,CD8+T亚群细胞升高,导致CD4+/CD8+比值下降并倒置;CD4+CD45RA+亚群、CD4+CD45RA+/CD4+CD45RO+比值下降,CD4+CD45RO+亚群上升;CD8+CD45RA+亚群、CD8+CD45RO+亚群和CD8+CD45RA+/CD8+CD45RO+比值均有所上升;自身免疫性疾病有关的CD4+CD28+亚群下降。结论 COPD患者体内存在细胞免疫功能的紊乱。     

老年SD大鼠脾脏和外周血T淋巴细胞亚群的变化

目的探讨SD老年大鼠脾脏和外周血T淋巴细胞亚群的变化。方法流式细胞仪检测老年大鼠(10只)和青年鼠(5只)脾脏和血液T淋巴细胞亚群的变化。结果 SD老年大鼠脾脏和外周血T淋巴细胞亚群阳性率的变化相一致,CD3+、CD4+、CD8+细胞阳性率均低于青年组水平,且CD4细胞阳性率均明显低于青年组(P<0.05);CD4+/CD8+比值均低于青年组,在脾脏CD4+/CD8+比值与青年组相比具有显著性差异(P<0.05)。结论 SD老年大鼠脾脏和外周血T胞亚群阳性率均减少,且CD4+/CD8+比值明显降低,提示SD老年大鼠免疫功能的衰退和紊乱与T细胞密切相关。     

急性心肌梗死患者冠状动脉支架置入前后外周血T细胞亚群构成变化

目的了解急性心肌梗死(AMI)患者冠状动脉支架置入前后外周血T细胞亚群CD3+、CD4+、CD8+水平的变化。方法纳入175例AMI并置入冠状动脉支架的患者,同时选择60例年龄、性别相匹配的的健康人群作为对照组。应用流式细胞技术分别对AMI患者支架置入术前、术后第1 d、第7 d以及对照组人群外周血T细胞亚群CD3+、CD4+、CD8+水平进行检测,比较AMI患者支架置入前后T细胞亚群水平变化及TMP心肌灌注分级对T细胞亚群水平的影响。结果 AMI组患者冠脉支架置入术前、术后1 d、7 d及对照组间血CD3+、CD4+、CD4+/CD8+水平呈增高趋势,而血CD8+水平呈降低趋势,组间差异有统计学意义(P0.05)。TMP2-3组CD3+、CD4+、CD4+/CD8+高于TMP0-1组,而CD8+低于TMP0-1组,差异有统计学意义(P均0.05)。结论 AMI患者外周血T细胞亚群构成异常,冠状动脉支架置入术后T淋巴细胞亚群构成明显改善。     

炎症性肠病患者T淋巴细胞亚群的改变及临床意义

目的探讨炎症性肠病(IBD)患者外周血T淋巴细胞亚群的变化特点及临床意义.方法对临床确诊的18例溃疡性结肠炎(UC)和9例Crohn病(CD)患者,于疾病的不同时期用荧光单克隆抗体标记-流式细胞仪技术检测其外周血T淋巴细胞亚群的变化,并结合临床和病理资料进行综合分析.结果UC患者缓解期时的CD3+、CD8+和自然杀伤(NK)细胞与对照组比较无显著差异;但活动期时,其CD8+和NK细胞数明显下降(CD8+活动期23.1%±1.0%,对照组31.3%±1.2%,P＜0.05;NK活动期9.8%±1.0%,对照组15.1%±1.1%,P＜0.01),CD4+/CDs+比值上升(活动期1.8±0.1,对照组1.4±0.02,P＜0.05);活动期CD患者的CD8+细胞和CD4+/CD8+比值(43.0%±44%和0.6±0.1)变化却与UC组活动期呈相反趋势(P＜0.01).结论T淋巴细胞亚群改变在IBD的发病机制中可能起重要作用;UC和CD的细胞免疫机制不同;外周血CD4+、CD8+、NK细胞和CD4+/CD8+比值可作为检测UC病情变化和疗效考核的敏感指标.     

慢性丙型肝炎外周血淋巴细胞亚群与HCV RNA载量及HCV抗体的相关性分析

目的探讨慢性丙型肝炎(CHC)患者外周血淋巴细胞亚群的变化以及与丙型肝炎病毒(HCV)病毒载量和抗HCV水平的相关性。方法应用流式细胞术检测60例慢性丙型肝炎患者外周血T淋巴细胞亚群及NK细胞的相对数量,与20例正常健康人做比较;应用实时荧光定量RT-PCR对其外周血HCV病毒载量进行检测,分为3组进行分析;化学发光法检测血清抗HCV水平,分2组进行比较分析。另外,分析HCV RNA载量及抗HCV水平与外周血淋巴细胞亚群变化的相关性。结果慢性丙型肝炎患者组外周血CD4+T淋巴细胞比例、NK细胞比例和CD4+/CD8+比值低于正常人组,CD8+T淋巴细胞比例高于正常人组;随着HCV RNA载量的增高CD4+、CD4+/CD8+比值及NK细胞比例逐渐降低,CD8+T淋巴细胞比例逐渐增高。随着抗HCV水平的增高CD4+、CD4+/CD8+比值及NK细胞比例逐渐降低,CD8+T淋巴细胞比例逐渐增高。结论 CHC患者细胞免疫功能存在着较严重的失调,随着HCV病毒复制和机体抗体水平的增高,患者的特异性和非特异性细胞免疫功能均越受到抑制,机体清除病毒的能力越弱,导致病毒不能有效的被清除,使病情反复迁延,造成HCV病毒持续感染,从而促进了HCV感染的慢性化及疾病的进展,少部分患者甚至发生了恶变导致肝细胞癌。     

乙型肝炎患者外周血T淋巴细胞亚群的变化

目的研究乙型肝炎患者外周血T淋巴细胞亚群变化及其临床意义.方法对140例乙型肝炎患者和64例健康者,采用特异性荧光抗体标记、流式细胞仪检测T淋巴细胞亚群的改变.结果与正常对照组比较,慢性肝炎、肝炎肝硬变、慢性重型肝炎患者外周血CD3+、CD4+、CD8+及CD4+/CD8+比值均有显著性下降(P＜0.05),以肝炎肝硬变下降最显著,急性乙型肝炎T细胞亚群数量和比值变化不明显(P＞0.05).HBV DNA(+)与HBV DNA(-)患者外周血T细胞亚群数量和比值变化比较无显著性差异(P＞0.05).结论乙型肝炎病毒感染后机体T淋巴细胞功能低下主要见于慢性病毒感染状态,其下降程度与病毒复制水平无明显关系.     

外周血T淋巴细胞亚群和慢性丙型肝炎患者HCV复制程度关系的研究

目的分析外周血T淋巴细胞亚群和慢性丙型病毒性肝炎(chronic hepatitis C,CHC)患者的丙型肝炎病毒(hepatitis C virus,HCV)复制程度的关系。方法选取上海市第七人民医院收治的CHC患者65例和健康体检者20名,流式细胞仪检测外周血中的T细胞亚群,荧光定量PCR法检测患者血清HCV RNA复制程度。结果 CD3+T细胞亚群在两组人群中分布相比,差异无统计学意义(P0.05);CD4+T细胞亚群在CHC患者中分布明显低于健康体检者(P0.05),而CD8+T细胞亚群在CHC患者中分布明显高于健康体检者(P0.05)。CD3+T细胞亚群百分率与HCV复制程度无明显相关性(P0.05);CD4+T细胞亚群、CD8+T细胞亚群百分率和CD4+/CD8+比值与HCV复制程度有明显相关性(P0.05)。结论 CHC患者外周血T淋巴细胞亚群比例改变与导致HCV感染慢性化密切相关。HCV RNA复制程度增加进一步导致T细胞亚群紊乱,CD4+/CD8+比值的动态变化可提示HCV感染者细胞免疫功能的变化。     

替比夫定对HBeAg阳性慢性乙型肝炎患者外周血T淋巴细胞亚群的影响

目的探讨替比夫定对HBeAg阳性慢性乙型肝炎(CHB)患者细胞免疫功能的影响。方法采用流式细胞术分别检测替比夫定治疗HBeAg阳性慢性乙型肝炎患者完全应答组55例、部分应答组71例、无应答组24例基线,治疗12周、24周、52周外周血T淋巴细胞亚群,同时检测30例健康体检者外周血T淋巴细胞亚群作为对照组。结果慢性乙型肝炎患者较正常对照组CD3+、CD4+、CD8+T细胞数以及CD4+/CD8+比值均降低(P<0.05)。治疗前完全应答组、部分应答组及无应答组的CD3+、CD4+、CD8+T细胞数及CD4+/CD8+比值各组之间的差异无统计学意义(P>0.05)。经替比夫定治疗后,CD3+、CD4+、CD8+T细胞数及CD4+/CD8+比值在完全应答组及部分应答组均较无应答组升高(P<0.05)。在完全应答组内CD3+、CD4+、CD8+T细胞数及CD4+/CD8+比值自服用替比夫定12周起及其后各时间点较基线时明显升高,差异具有统计学意义(P<0.05);在部分应答组内CD3+、CD4+T细胞数及CD4+/CD8+比值从服用替比夫定24周起较基线时明显升高,差异具有统计学意义(P<0.05);而无应答组治疗各时间点与基线相比较,CD3+、CD4+、CD8+T细胞数及CD4+/CD8+比值均无明显变化(P>0.05)。结论慢性乙型肝炎患者经替比夫定治疗后可抑制其HBV复制,替比夫定可改善慢性乙型肝炎患者的细胞免疫功能。     

老年肺癌患者外周血T淋巴细胞亚群和自然杀伤细胞的临床及意义

目的探讨老年肺癌患者T淋巴细胞亚群和自然杀伤(NK)细胞水平及临床意义。方法该校附属医院80例老年肺癌患者作为观察组,回顾分析外周血T淋巴细胞亚群和NK细胞检测结果,与另选的80例健康受检者(对照组)进行对比分析,并于术后20 d复查肺癌患者的外周血T淋巴细胞亚群和NK细胞,对比缓解者与未缓解者的检查结果。结果外周血T淋巴细胞亚群与NK细胞表达水平检测中,观察组CD3+、CD4+、CD4+/CD8+比值与NK细胞水平较对照组明显降低(P0.05),CD8+表达水平明显高于对照组(P0.05)。观察组于术后20 d复查T细胞亚群和NK细胞,根据结果分为两组进行分析,发现缓解组CD3+、CD4+、CD4+/CD8+和NK表达均较化疗前明显上升,CD8+表达显著降低(P0.05)。而未缓解组各项指标化疗前后无明显变化(P0.05)。结论 NK细胞与外周血T淋巴亚群对诊断、评价肺癌的疗效、判断预后具有重要价值。     

冠心病患者外周血T淋巴细胞及其亚群分析

应用抗人T淋巴细胞单克隆抗体CD系列检测30例冠心病患者外周血T淋巴细胞亚群CD_3~+、CD_4~+、CD_8~+及CD_4~+/CD_8~+比值,并与正常健康人对照组比较。经间接免疫SPA法测定,冠心患者CD_3~+、CD_4~+及CD_4~+/CD_8~+比值均较对照组明显降低(P<0.05～0.001),而冠心病患者中急性心肌梗塞、心绞痛组与隐性冠心病组之间却无明显差别(P>0.05)。文中就T细胞亚群CD_4~+降低对冠心病发生机制作了初步探讨。     

Effect of viral load on T-lymphocyte failure in patients with chronic hepatitis B

AIM： To investigate peripheral T-lymphocyte sub-population profile and its correlation with hepatitis B virus （HBV） replication in patients with chronic hepatitis B （CHB）.METHODS： Distribution of T-lymphocyte subpopulations in peripheral blood was measured by flow cytometry in 206 CHB patients. HBV markers were detected with ELISA. Serum HBV DNA load was assessed with quantitative real-time polymerase chain reaction （PCR）. The relationship between HBV replication and variation in peripheral T-cell subsets was analyzed.RESULTS： CHB patients had significantly decreased CD3^＋ and CD4^＋ cells and CD4^＋/CD8^＋ ratio, and increased CD8^＋ cells compared with uninfected controls （55.44 ± 12.39 vs 71.07 ± 4.76, 30.92 ± 7.48 vs 38.94 ± 3.39, 1.01 ± 0.49 vs 1.67 ± 0.33, and 34.39 ± 9.22 vs 24.02 ± 4.35; P 〈 0.001, respectively）. Univariate analysis showed a similar pattern of these parameters was significantly associated with high viral load, presence of serum hepatitis B e antigen （HBeAg） expression, liver disease severity, history of maternal HBV infection, and young age at HBV infection, all with P 〈 0.01. There was a significant linear relationship between viral load and these parameters of T-lymphocyte subpopulations （linear trend test P 〈 0.001）. There was a negative correlation between the levels of CD3＋ and CD4＋ cells and CD4^＋/CD8^＋ ratio and serum level of viral load in CHB patients （r = -0.68, -0.65 and -0.75, all P 〈 0.0001）, and a positive correlation between CD8^＋ cells and viral load （r = 0.70, P 〈 0.0001）. There was a significant decreasing trend in CD3^＋ and CD4^＋ cells and CD4^＋/CD8^＋ ratio with increasing severity of hepatocyte damage and decreasing age at HBV infection （linear trend test P 〈 0.01）. In multiple regression （after adjustment for age at HBV infection, maternal HBV infection status and hepatocyte damage severity） log copies of HBV DNA maintained a highly significant predictive coefficient on T-lymphoc     

Tc2 response at the onset of COPD exacerbations

BACKGROUND: T lymphocytes and especially the subpopulations of CD8+ cells are believed to have a key role in COPD pathophysiology, but there are only few data regarding the role of these cells in COPD exacerbation. Aim: We aimed to study prospectively changes of CD8+ T-lymphocyte subpopulations in the sputum of COPD patients at the onset of mild exacerbations and at a stable condition in order to provide further insight in the pathophysiology of the disease. METHODS: Induced-sputum samples were collected from 24 COPD patients with median age of 52 years (interquartile range [IQR], 44 to 58 years) and FEV(1) percentage of predicted of 78.05% (IQR, 75.8 to 80.1%) at the onset of mild exacerbations not requiring hospitalization and when stable. Inflammatory cells and T-lymphocyte subpopulations (CD4+, CD8+, and cells producing interferon [IFN]-gamma or interleukin [IL]-4) were measured using flow cytometry and immunocytochemical methods. RESULTS: A significant increase in sputum CD8+ T lymphocytes (p < 0.0001) and significant decreases in CD4+ T lymphocytes as well as in CD4+/CD8+ (p = 0.0001) and CD8+IFN-gamma+/CD8+IL-4+ (p = 0.001), CD4+IFN-gamma+/CD4+IL-4+ (p = 0.0003) sputum cells ratios were found decreased at the onset of exacerbations compared to stable condition. The changes in T-lymphocyte subpopulations were not associated with smoking history, demographic characteristics, or disease severity. CONCLUSION: The findings of the present study suggest that CD8+ lymphocytes are increased and potentially polarized toward a Tc2 profile in the airways of COPD patients at the onset of COPD exacerbations with respect to stable condition. The clinical impact of the observed phenomenon requires further investigation.     

Changes in sputum T-lymphocyte subpopulations at the onset of severe exacerbations of chronic obstructive pulmonary disease

CD8+ve T-cell responses play a primary role in chronic obstructive pulmonary disease (COPD), but there is little information regarding COPD exacerbations. Sputum induction is a relatively non-invasive and safe method to study airway inflammation. The aim of the study was to investigate changes in airway T-lymphocyte subpopulations at the onset of severe COPD exacerbations via analysis of sputum. Induced sputum samples were collected from 12 COPD patients aged (mean+/-sd) 69+/-7 years, ex-smokers (68+/-23 pack-years), mean FEV1 (%predicted) 40+/-14 at the onset of an acute severe exacerbation requiring hospital admission and 16 weeks after remission of the exacerbation. Inflammatory cells and T-lymphocyte subpopulations (CD4, CD8, Tc1, Tc2) were measured using chemical and double immunocytochemical methods. Increased percentages of sputum neutrophils (P=0.002) and decreased CD4/CD8 and CD8-IFNgamma/CD8-IL4+ve (Tc1/Tc2) cell ratios (P=0.03, P=0.02, respectively) were found at the onset of exacerbation compared to stable state. We conclude that a CD8+ve type-2-mediated immune response is induced at the onset of severe COPD exacerbation.     

乙型肝炎病毒核心区基因变异与细胞免疫

目的 探讨慢性乙型肝炎患者乙型肝炎病毒(HBV)核心区Leu60Val变异与机体细胞免疫水平的关系。方法 通过流式细胞分析技术(FCM)检测外周血T淋巴细胞亚群,利用酶联免疫吸附试验(ELISA)检测血清细胞因子[干扰素γ(IFN-γ)、肿瘤坏死因子α(TNF-α)和白细胞介素2(IL-2)]水平,采用聚合酶链反应(PCR)扩增HBV DNA C基因区片段,并对PCR产物直接测序。结果 91例慢性乙型肝炎患者发生Leu60Val变异者19例,变异率为20.9％,随病情加重变异率逐渐增加,以重型肝炎组最高;Val60变异株组IFN-γ、TNF-α水平明显增高(t值分别为2.584、4.766,P<0.01),CD_4~1/CD_8~1比值逐渐升高(t=2.275,P<0.05)。结论 Val60变异株可能通过增加与Ⅰ类人白细胞抗原(HLA-Ⅰ)的亲和力,或上调HLA-Ⅰ类分子的表达,从而激活大量的细胞毒性T淋巴细胞释放细胞因子,并同时在肝脏局部发挥免疫效应,提高对宿主的杀伤力。     

Relationship of BAL and lung tissue CD4+ and CD8+ T lymphocytes, and their ratio in idiopathic pulmonary fibrosis

BACKGROUND: Surgical biopsy specimens have shown that T lymphocytes (TLs) infiltrate lung parenchyma in patients with idiopathic pulmonary fibrosis (IPF) and might play a pathogenetic role. BAL, a far less invasive technique, has also been used for the investigation of IPF pathogenesis. However, controversy exists whether the BAL fluid cellular profile reflects the cellular composition of the lung parenchyma. STUDY OBJECTIVE: To compare infiltrating TLs subpopulations (CD4+, CD8+, and CD4+/CD8+ ratio) in lung tissue and BAL fluid. PATIENTS AND METHODS: Immunohistochemistry was performed according to the streptavidin-biotin method on the surgical biopsy specimens of 12 untreated patients with IPF. The number of CD3+, CD4+, and CD8+ TLs was determined by observer-interactive computerized image analysis (SAMBA microscopic image processor; Meylan, France). In BAL fluid, the same TLs subpopulations were evaluated by flow cytometry. RESULTS: In lung tissue, CD3+ TLs accounted for a mean (+/- SEM) of 28.8 +/- 7% of total cells, CD4+ TLs accounted for 14.5 +/- 4% of total cells (50.1 +/- 4% of CD3+ TLs), and CD8+ TLs accounted for 13.8 +/- 4% of total cells (47.4 +/- 4% of CD3+ TLs). In BAL fluid, lymphocytes accounted for 9.8 +/- 2.5% of total cells, CD4+ TLs accounted for 51.8 +/- 4% of CD3+ TLs, and CD8+ TLs accounted for 42.2 +/- 4% of CD3+ TLs. Tissue CD4+ and CD8+ TLs (expressed as a percentage of CD3+ TLs) correlated significantly with the number of CD4+ and CD8+ TLs in BAL fluid (r = 0.846 and p = 0.001 vs r = 0.692 and p = 0.013, respectively). A significant positive correlation was also found between the mean CD4+/CD8+ ratio found in tissue and BAL fluid (1.05 +/- 0.21 and 1.5 +/- 0.27, respectively; r = 0.832; p = 0.01). CONCLUSION: The results suggest that in patients with IPF, the TL subpopulations in BAL fluid reflect the pattern of lymphocytic infiltration in pulmonary parenchyma.     

Circulating T-lymphocyte activation in patients with variant angina

BACKGROUND: Both experimental and pathological studies suggest that immune response and inflammation may play an important role in the pathogenesis of coronary spasm. DESIGN: To elucidate the role of systemic immune and inflammatory responses in the pathogenesis of coronary spasm, we studied circulating T-lymphocyte activation in variant angina patients (VAPs), stable effort angina patients (EAPs) and in control participants. METHODS: Twenty documented VAPs, 13 EAPs and 20 control participants were studied. To evaluate T-lymphocyte activation, T-lymphocyte surface antigen expression, including CD3, CD4, CD8 and HLA-DR, was measured by two-colour flow cytometric analysis. Serum-soluble interleukin-2 receptor (sIL-2R) and C-reactive protein (CRP) were also measured by enzyme-linked immunosorbent assay. We restudied 10 of the VAPs to investigate the relationship between the disease activity of variant angina and T-lymphocyte activation. RESULTS: The percentage of CD3+/DR+ T-lymphocytes in VAPs (14.8%) was significantly higher than in EAPs (10.7%, P < 0.05) and control participants (9.7%, P < 0.005); however, levels of sIL-2R were the same among the three groups. Levels of CRP were within normal range in all VAPs. The percentage of CD8+/DR+ T-lymphocytes was significantly higher in VAPs (9.5%, P < 0.005) than in EAPs (5.5%) and control participants (5.9%), whereas the percentage of CD4+/DR+ T-lymphocytes was similar among the three groups. The percentage of activated T-lymphocytes in VAPs was unchanged during the follow-up period (mean intervals, 10 months). CONCLUSIONS: These results indicate that the chronic activation of T-lymphocytes, especially CD8+ T-lymphocytes, may be involved in the pathogenesis of coronary spasm.     

冠状动脉粥样硬化性心脏病患者T淋巴细胞亚群的变化及意义

目的 探讨冠状动脉粥样硬化性心脏病(冠心病)患者外周血T淋巴细胞亚群数量和比例变化特征及意义.方法 入选2016年1月至2018年12月南京医科大学附属南京医院254例冠心病患者,其中急性心肌梗死80例、不稳定型心绞痛84例和稳定型心绞痛90例,另外选择同期79例胸痛综合征患者设为对照组.流式细胞分析法检测各组患者总T...     

温下法与温涩法对溃疡性结肠炎外周血T淋巴细胞亚群的影响

[目的]探讨温下法与温涩法在溃疡性结肠炎（UC）细胞免疫调节方面的不同作用机制。[方法]采用流式细胞仪三色标记法检测治疗前后温下组、温涩组和对照组的外周血T淋巴细胞亚群的水平，比较3组治疗前后的变化。[结果]治疗前，温下组、温涩组和对照组外周血CD8^＋细胞绝对计数均显著高于正常参考值（P〈0．05），CD4^＋／CD8^＋比值均显著低于正常参考值（P〈0．05）；温下组与对照组外周血CD3^＋、CD4^＋细胞绝对计数亦显著高于正常参考值（P〈0．05）。治疗后，温下组外周血CD3^＋、CD4^＋与CD8^＋细胞绝对计数变化差值均显著高于温涩组与对照组（P〈0．01）；温涩组外周血CD3^＋与CD8^＋细胞绝对计数变化差值均显著高于对照组（P〈0．01），CD4^＋／CD8^＋比值变化差值高于温下组与对照组（P〈0．05）。[结论]①UC患者外周血T淋巴细胞亚群的变化总体以CD8^＋细胞水平升高及CD4^＋／CD8^＋比值下降为主，而CD4^＋细胞绝对数增多与其活动性有关。②温涩法不但能显著降低CD3^＋细胞计数和CD8^＋细胞计数，还能提高CD4^＋／CD8^＋比值；温下法能显著降低CD3^＋、CD4^＋与CD8^＋细胞计数，但不能提高CD4^＋／CD8^＋比值。     

Serum C-reactive protein elevation in left ventricular remodeling after acute myocardial infarction--role of neurohormones and cytokines

BACKGROUND: We previously reported that increased peak serum C-reactive protein (CRP) level after acute myocardial infarction (AMI) was a major predictor of cardiac rupture and long-term outcome. The aim of this study was to clarify the role of serum CRP elevation as a possible marker of left ventricular (LV) remodeling after AMI. METHODS: We prospectively studied 31 patients who underwent primary angioplasty for a first anterior Q-wave AMI. Peak serum CRP level was determined by serial measurements after admission. LV volume and the plasma levels of various neurohormones and cytokines were measured on admission, and 2 weeks and 6 months after AMI. RESULTS: Patients with higher peak CRP levels (above the median) had a greater increase in LV end-diastolic volume during 2 weeks after AMI (+21+/-14 vs. +5+/-6 ml/m(2), P=0.001) and a lower ejection fraction (45+/-11 vs. 53+/-7%, P=0.02) than those with lower CRP levels, associated with a higher incidence of pump failure, atrial fibrillation, and LV aneurysm. Plasma levels of norepinephrine, brain natriuretic peptide, and interleukin-6 2 weeks after AMI were higher in the high CRP group than in the low CRP group. CONCLUSIONS: Increased peak serum CRP level was associated with a greater increase in LV volume after anterior AMI. Plasma norepinephrine and interleukin-6 levels were increased in patients with higher CRP levels, suggesting a possible role of sympathetic activation and enhanced immune response in the development of LV remodeling after AMI.     

Abnormal peripheral blood T-lymphocyte subsets in a subgroup of patients with COPD

BACKGROUND: Smoking may induce changes in T-lymphocyte subsets in peripheral blood. Abnormalities of T-lymphocyte subsets in peripheral blood and in BAL fluid, and increased CD8+ T lymphocytes in the airways have been reported in patients with COPD. These findings suggest that T-lymphocyte abnormalities might be involved in the pathogenesis of airflow limitation in people who smoke. DESIGN: Cross-sectional study. SETTING: Outpatient pulmonary department of a university hospital. METHODS: To investigate this hypothesis, peripheral blood T-lymphocyte subsets were measured by flow cytometry using specific monoclonal antibodies in 20 healthy nonsmokers, 20 healthy smokers, and 20 smokers with stable COPD. No significant differences in the peripheral blood T-lymphocyte subsets were observed among the three groups. Because a previous study showed peripheral blood T-lymphocyte abnormalities in the subgroup of nonsmoking patients with COPD, we wanted to investigate what factors determine the subgroup of COPD with abnormal T-lymphocyte subsets. We tried to measure the relationship between T-lymphocyte subsets and physiologic indexes of pulmonary function tests in patients with COPD. The proportion of CD8+ T lymphocytes significantly correlated with diffusing capacity of the lung for carbon monoxide (DLCO) and DLCO per unit of alveolar volume (DLCO/VA), and CD4+/CD8+ ratio correlated with DLCO/VA. Therefore, we attempted to classify the patients with COPD into two subgroups on the basis of DLCO/VA: 10 COPD patients with low DLCO/VA (< 80% predicted) and 10 patients with normal DLCO/VA (> or = 80% predicted). RESULTS: The normal DLCO/VA subgroup had a significantly higher proportion of CD8+ T lymphocytes and a lower CD4+/CD8+ ratio than the healthy smokers or the low DLCO/VA subgroup. Moreover, FEV1/FVC significantly correlated with the CD4+/CD8+ ratio only in the normal DLCO/VA subgroup. CONCLUSION: These findings suggest that T-lymphocyte abnormalities might be involved in the pathogenesis of airflow limitation in a subgroup of patients with COPD, presumably with small airways disease, but not in all cases of COPD.