ω-3多不饱和脂肪酸对急性呼吸窘迫综合征患者血清炎症介质的影响

目的观察ω-3多不饱和脂肪酸对急性呼吸窘迫综合征（ARDS）患者血清炎症介质释放的影响。方法将42例ARDS患者按随机化数字表原则,分为对照组和研究组,每组各21例。两组患者均接受等氮、等热量的全胃肠外营养,热量25kcal·kg^-1·d^-1、氮摄入量0.2g/kg,其中研究组加用ω-3多不饱和脂肪酸（0.2g·kg^-1·d^-1）,共7d。分别检测治疗前和治疗后第1、3、7天血清白细胞介素1（IL-1）、IL-6、肿瘤坏死因子α（TNF-α）水平,并观察动脉血氧分压和氧合指数的变化。结果加用ω-3多不饱和脂肪酸治疗后,研究组在不同时间点IL-1、IL-6、TNF-α均明显低于对照组（P均〈0.05）;两组患者动脉血氧分压和氧合指数均有改善,且研究组氧合指数较高,差异均有统计学意义（P均〈0.05）。结论ω-3多不饱和脂肪酸可降低ARDS患者IL-1、IL-6、TNF-α水平,在一定程度上有利于ARDS患者呼吸功能的恢复。     

不同缺血后处理对缺血再灌注大鼠脑内IL-1β、IL-6表达的影响

目的对局灶性缺血/再灌注大鼠实施不同缺血后处理,观察其对大脑炎症介质释放的影响,为其对缺血性脑损伤的保护提供依据。方法成年SD大鼠25只,采用线栓法制作大鼠大脑中动脉缺血/再灌注模型,随机分为5组,分别为假手术组、缺血再灌注组、缺血后处理组、远隔后处理组、延迟后处理组,术后48 h取脑组织,用免疫组化法观察缺血侧皮质和海马内IL-1β、IL-6表达及相同部位轴突形态。结果和缺血/再灌注组相比,缺血后处理和远隔后处理组损伤侧皮质和海马缺血范围减小,局部炎症反应减轻,轴突损伤减少。结论大鼠局灶性脑缺血/再灌注损伤后早期进行缺血后处理可显著减少大脑炎症反应,使轴突的损伤情况改善。     

老年急性重症胆源性胰腺炎的早期内镜治疗

目的探讨早期急诊内镜治疗对老年急性重症胆源性胰腺炎的临床价值。方法确诊为急性重症胆源性胰腺炎的92例高龄患者,分成内镜组（n=43）和对照组（n=49）,对其血清肿瘤坏死因子（TNF）-α、白细胞介素（IL）-6、IL-8以及淀粉酶恢复正常时间、腹痛缓解时间、住院天数,还有并发症发生率和死亡率等指标进行比较分析。结果治疗7d后内镜组患者血清TNF-α、IL-6、IL-8和对照组比较下降更明显,差异有统计学意义[（45．16±13．48）μg／L比（176．89±47．35）μg／L、（31．76±13．85）μg／L比（68．48±24．87）μg／L、（113．39±63．78）μg／L比（309．86±117．13）μg／L,P均〈0．05];内镜组患者腹痛缓解时间、淀粉酶恢复正常时间、住院时间明显短于对照组[（10．2±1．7）d比（13．2±2．4）d、（3．3±1．0）d比（5．5±1．2）d、（15±1．6）d比（20±3．0）d,P均〈0．05];并发症发生率也低于对照组（5％比22％,P〈0．05）。结论早期内镜介入治疗老年急性重症胆源性胰腺炎具有微创、安全、有效的优点,能明显缓解病情的进一步发展。     

血清白细胞介素-33与类风湿关节炎合并肺间质病变相关性研究

目的 分析类风湿关节炎(RA)合并肺间质病变(ILD)患者血清白细胞介素(IL)-33及其受体人基质裂解素2(ST2)的表达情况及与肺功能等实验室指标的相关性,为其早期诊断提供依据.方法 收集2012年3月至2013年3月在我科初诊为RA患者245例,分为RA-ILD组58例与单纯RA组187例,观察各组肺功能等相关实验室指标,另收集我院体检中心健康体检者60名为健康对照组.采用酶联免疫吸附试验(ELISA)法测定以上各组的血清IL-33及ST2浓度水平.组间比较采用两样本t检验;多组间比较采用多个样本均数比较的方差分析;IL-33浓度及相关变量间比较采用Pearson相关分析.结果 RA患者ILD发生率为23.7％(58/245).与健康对照组[(85±38) pg/ml]相比,RA[(433±42) pg/ml]及RA-ILD [(746±43) pg/ml]患者中血清IL-33水平显著增高,差异有统计学意义(P＜0.01);且与RA组患者相比,RA-ILD组患者血清IL-33及ST2水平升高更为明显(P＜0.01).RA-ILD组患者肺活量占预计值百分比(VC％)、用力肺活量占预计值百分比(FVC％)、最大呼气中段流量占预计值百分比(MMF％)和一氧化碳弥散量(DLCO)多项肺功能指标均较RA组患者明显降低,差异有统计学意义(P＜0.01).IL-33浓度与各实验室指标相关性比较:IL-33浓度与类风湿因子呈正相关(r=0.82,P＜0.01),且与抗环瓜氨酸多肽抗体(ACPA)滴度呈正相关(r=0.55,P＜0.01),而其与DLCO呈负相关(r=-0.80,P＜0.01).结论 IL-33参与RA的发病过程,且可能与RA-ILD的发病相关.     

无免疫功能低下的肺隐球菌病患者Th1/Th2类细胞因子的变化

目的 分析无免疫功能低下的肺隐球菌病(PC)患者Th1/Th2类细胞因子的变化及其机制.方法 应用酶联免疫吸附测定(ELISA)法测定20例无免疫功能低下的PC患者(PC组)血清中IL-12、γ-干扰素(IFN-γ)和IL-4的浓度,并与20名健康体检者(对照组)进行对比.分离PC组和对照组外周血单个核细胞(PBMC),重组人IL-12 (rhIL-12)刺激48 h后收集上清液,应用ELISA法测定各组培养上清液中IFN-γ和IL-4的浓度.结果 (1)无免疫功能低下的PC患者血清IFN-γ的浓度为(14.5±2.7) ng/L,显著低于对照组的(81.8±9.8) ng/L,差异有统计学意义(t=6.590,P＜0.01),PC组和对照组血清IL-12浓度分别为(2.5±0.5)和(2.5±0.6) ng/L,血清IL-4浓度分别为(6.9±1.3)和(7.3±1.5) ng/L,差异均无统计学意义(t值分别为0.0035和0.2136,均P＞0.05).(2)PC组与对照组PBMC上清液中IFN-γ浓度分别为(55.7 ±13.6)和(51.1±17.5) ng/L,IL-4分别为(5.1±0.7)和(5.0±0.6)ng/L,差异均无统计学意义(t值分别为0.2979和0.0325,均P＞0.05).(3)经rhIL-12刺激后,PC组和对照组PBMC上清液中IFN-γ的浓度均有明显增高,为(4.3±0.5)和(7.9±1.1)倍,PC组增高幅度明显低于对照组,差异有统计学意义(t=3.01,P＜0.01);而IL-4的浓度两组分别增加了(0.9±0.4)和(1.3±0.4)倍,差异无统计学意义(t=0.7240,P＞0.05).结论 无免疫功能低下的PC患者血清Th1类因子(IFN-γ)下降,Th2类因子(IL-4)无明显变化;Th1细胞对IL-12的反应性和敏感性下降可能是血清Th1类因子(IFN-γ)下降的原因之一.     

白细胞介素类mRNA在儿童哮喘中异常表达的检测及意义

目的：研究白细胞介素－12（IL－12），IL－13在哮喘发病中的作用。方法：用逆转录聚合酶链反应（RT－PCR）法半定量分析了哮喘急性发作期及正常对照组儿童外周血单个核细胞（PBMC）中IL－12，IL－13mRNA表达水平的变化，同时对IgE水平进行了检测，结果：哮喘组IL－12 mRNA表达减少，IL－13 mRNA表达增多，病情越重，IL－12mRNA表达越少，IL－13 mRNA表达越多，无论IgE升高与否。与对照组比较，IL－12，IL－13mRNA表达，差异均有显著性，结论：IL－12，IL－13可能是构成气道慢性炎症的各类因素之一。     

Immunosenescence and inflammation characterize chronic heart failure patients with more advanced disease

Background

Chronic heart failure (CHF) is characterized by an inflammatory status with high levels of cytokines such as IL-6. We hypothesized that patients with CHF may develop immunosenescence due to inflammation and that this may be associated with a worse stage of the disease.

Methods and results

We compared the immunological features of 58 elderly CHF patients (ECHF), 40 young CHF patients (YCHF), 60 healthy elderly controls (HEC) and 40 healthy young controls (HYC). We characterized leukocyte and lymphocyte subpopulations by flow cytometry, and IL-6 concentration by ELISA. The extent of CHF was classified according to functional and/or morphological criteria: New York Heart Association functional class, AHA/ACC heart failure stages, left ventricular ejection fraction, and left ventricular hypertrophy. CHF patients showed an increased number of leukocytes, neutrophils and monocytes, but a decreased number of lymphocytes. CHF patients had significantly lower levels of B-cells and CD4 + T-cells, increased NK-cells in YCHF, and increased CD8 + T-cells only in ECHF. CHF was associated with high differentiation in CD4 + and CD8 + T-lymphocyte subsets. Aging of T-lymphocyte subpopulations and high IL-6 levels were associated with a worse clinical status. IL-6 also correlated positively with the number of highly differentiated T-lymphocytes and with their accelerated aging.

Conclusions

We conclude that CHF patients show a higher degree of immunosenescence than age-matched healthy controls. T-lymphocyte differentiation and IL-6 levels are increased in patients with an advanced clinical status and may contribute to disease impairment through a compromised adaptive immune response due to accelerated aging of their immune system.     

Study of pro-inflammatory (TNF-α, IL-1α, IL-6) and T-cell-derived (IL-2, IL-4) cytokines in plasma and synovial fluid of patients with juvenile chronic arthritis: Correlations with clinical and laboratory parameters

Acute phase proteins, synovial fluid (SF) cellular infiltrates, pro-inflammatory (TNF-, IL-1, IL-6) and Th1 (IL-2) and Th2 (IL-4) derived cytokine levels both in plasma and SF were examined in pauciarticular and polyarticular juvenile chronic arthritis (JCA) patients during the active (n=22) and inactive (n=14) period in order to determine pathogenic mechanisms and correlations between cytokines and laboratory parameters showing disease activity. The erythrocyte sedimentation rate (ESR), serum C-reactive protein (CRP) and IgG concentrations were found to be significantly elevated in the active period of JCA. In pauciarticular JCA patients, when compared with their peripheral blood lymphocyte subpopulations, SF CD3+ cells (73.1%) and HLA-DR+ active T cells (22.5%) were found to be significantly increased. In the active period of JCA, plasma TNF- and IL-6 concentrations were significantly elevated. Plasma IL-2 and IL-4 levels were not elevated and were found to be similar to those in the inactive phase and in healthy controls. SF IL-6, TNF- and IL-1 levels were extremely high in all the patients. SF IL-4 and IL-2 levels were all undetectable. There was a significant correlation between ESR values and plasma IL-6 levels and between serum CRP levels and plasma IL-6 and TNF- concentrations. In conclusion, increased local production of pro-inflammatory cytokines appears to account for the articular manifestations of JCA. The impaired production of anti-inflammatory Th2-derived cytokines (IL-4) seems to cause increased production of inflammatory cytokines acting on the balance between them. The deficit in IL-2 production was not suggested to be primarily involved in the pathogenesis. In addition, not only CRP and ESR values, but also plasma IL-6 and TNF- concentrations may be used as markers of disease activity.     

白细胞介素与支架内再狭窄

支架置入术后的支架内再狭窄是困扰动脉粥样硬化性心脑血管病微侵袭介入治疗发展的主要问题.支架置入术后的血管内炎症反应是再狭窄的重要原因之一.其中,以白细胞介素为代表的细胞因子起着复杂和多变的作用.文章综述了白细胞介素表达水平对血管内皮增生的作用以及对支架内再狭窄发生率的影响.     

静脉注射丙种球蛋白无反应型川崎病Th17细胞的变化及意义

目的 探讨Th17细胞在静脉注射丙种球蛋白(IVIG)无反应型川崎病(KD)免疫发病机制中的作用.方法 选取KD患儿45例,其中IVIG敏感型KD 35例,IVIG无反应型KD 10例,同年龄健康对照组30名.KD患儿分别于IVIG治疗前后直接取血备检,IVIG无反应型KD分别在病程第8、9、11天取血备检.采用实时荧光定量聚合酶链反应(PCR)检测CD4~+T细胞白细胞介素(IL)-17A/F、转录因子ROR-γt mRNA表达;采用流式细胞术检测外周血Th17细胞占CD4~+T细胞比例.应用酶联免疫吸附试验(ELISA)检测Th17细胞相关的细胞因子IL-17A和IL-6的表达.结果 ①急性期KD患儿CD4~+T细胞IL-17A/F表达明显高于对照组(P<0.01);②急性期IVIG无反应型KD患儿CD4~+T细胞内IL-17蛋白、IL-17A/F mRNA、Th17细胞转录因子ROR-γt的基因表达明显高于IVIG敏感型KD,经IVIG治疗后敏感型KDTh17细胞相关因子表达明显降低(P<0.01),无反应型KD Th17细胞相关因子仍持续高表达(P>0.05);③急性期KD患儿治疗前IL-17A和IL-6血浓度明显高于对照组(P<0.01),其中IVIG无反应型KD活化细胞因子水平明显高于1VIG敏感型KD组(P<0.01).经治疗后均有下降趋势,但IVIG无反应型KD仍高于敏感型KD(P<0.01);④甲泼尼龙冲击治疗IVIG无反应型KD当天退热.血浆IL-6,IL-17A较前明显降低,C反应蛋白(CRP)恢复快,能够迅速控制血管炎性反应.结论 Th17细胞过度活化可能是导致IVIG无反应型KD的原因之一.