血清IL-6、IL-8和TNF—α在重症急性胰腺炎早期诊断中的临床意义

目的 对血清白介素-6(IL-6)、白介素-8(IL-8)及肿瘤坏死因子-α(TNF-α)等细胞因子在早期诊断重症急性胰腺炎(severe acute pancreatitis，SAP)中的价值进行研究。方法 以Ranson和APACHE—Ⅱ评分为标准，把36例急性胰腺炎患者分成轻症胰腺炎组(MAP)及重症胰腺炎组(SAP)两组，选择年龄匹配的13名健康志愿者为对照组(Con)；在患者入院24h内采静脉血并检测血清中IL-6、IL-8和TNF-α水平。结果 三种细胞因子血清水平均为SAP组最高，Con组最低，其中IL-6水平在三组之间、两两之间均有显著差异，IL-8和TNF—α水平在Con组与SAP组之间、MAP组与SAP组之间有显著差异，而Con组与MAP组之间无显著差异。结论 IL-6、IL-8、TNF—α对早期诊断鉴别轻症胰腺炎和重症胰腺炎均有重要的临床意义。     

急性胰腺炎患者血清TNF-α、IL-6及IL-8水平测定及分析

目的 观察TNF-α、IL-6及IL-8在急性胰腺炎（AP）发病中的作用。方法 对60例AP患者（AP组）分别于入院时及治疗7d后抽取空腹肘静脉血,采用放射性免疫法检测血清及TNF-α、IL-6及IL-8水平,同时选择20例健康体检者作为对照组。结果 AP组入院时血清TNF-α、IL-6及IL-8水平均显著高于对照组,其中重症（SAP）者显著高于轻症（MAP）者（P均〈0．05）;治疗7d后AP组上述指标均明显低于入院时,其中SAP患者仍显著高于对照组（P均〈0．05）。结论TNF-α、IL-6及IL-8均与AP发生、发展密切相关;检测其血清水平有助于AP早期诊断、病情判断和疗效观察。     

血清白细胞介素-6和细胞间黏附分子-1对急性胰腺炎严重程度的早期判断价值

目的:研究血清白细胞介素-6(IL-6)和细胞间黏附分子-1(ICAM-1)对急性胰腺炎严重程度的早期判断价值.方法:收集临床确诊的28例急性胰腺炎(AP)患者,分为重症急性胰腺炎(SAP)13例和轻症急性胰腺炎(MAP)15例两组,另选择10例体检健康人群作对照组(CG),分别测定血清IL-6和ICAM-1的浓度、并进行比较.结果:(1)发病24 h 内入院的SAP患者血清IL-6和ICAM-1浓度与MAP患者及对照组之间有显著性差异(P＜0.01);而MAP患者与CG之间无显著性差异(P＞0.05)(2)入院时SAP患者血清IL-6浓度与MAP患者及对照组之间有明显差异(P＜0.01);入院后SAP患者的血清IL-6浓度逐渐下降,5 d后与MAP比较无显著性差异(P＞0.05).(3)入院2 d后 SAP患者血清ICAM-1的浓度升高最明显,以后逐渐下降,但与MAP比较均有显著性差异(P＜0.05).讨论:血清IL-6和ICAM-1对急性胰腺炎病情严重程度有早期判断价值.     

胆汁中IL-6、TNF-α、IL-8检测对急性胆管炎诊断和严重程度的判断价值

目的探讨胆汁中白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、白细胞介素-8(IL-8)对急性胆管炎(AC)诊断和严重程度判断的价值。方法42例患者经ERCP胆道插管和/或术中抽取胆汁检测IL-6、TNF-α、IL-8的表达水平。结果AC患者轻症组与重症组胆汁中IL-6、TNF-α、IL-8的表达均显著高于对照组,重症组IL-6、TNF-α高于轻症组(P<0.001),重症组IL-8高于轻症组,但其差别无统计学意义(P>0.05)。结论胆汁中TNF-α、IL-6、IL-8参与了AC发病的病理过程,对AC的明确诊断以及严重程度预测有一定的价值。     

同型半胱氨酸、肿瘤坏死因子-α和白细胞介素-6对急性胰腺炎严重程度及预后的评价

目的 探讨同型半胱氨酸（HCY）、肿瘤坏死因子（TNF）-α和白细胞介素（IL）-6与急性胰腺炎（AP）病情严重程度的相关性以及对AP患者预后的评估价值.方法 选取AP患者64例,将其分为轻症AP组41例（MAP组）、重症AP组23例（SAP）;另选取健康体检者72例作为对照组.分别于入院第1、3和7天抽取静脉血检测血清HCY、TNF-α和IL-6水平,同时进行急性生理和慢性健康评分标准Ⅱ（APACHEⅡ）评分.结果 与对照组比较,入院第1天MAP组和SAP组血清HCY、TNF-α和IL-6水平均升高（P＜0.01）,其中SAP组升高更加明显（P＜0.01）;入院第3天时MAP组和SAP组血清HCY、TNF-α和IL-α水平均明显升高达到峰值;经常规治疗后（入院第7天）,两组HCY、TNF-α和IL-6水平均明显下降.HCY、TNF-α和IL-6水平与APACHEⅡ评分呈正相关（P＜0.01）.结论 血清HCY、TNF-α和IL-6水平与AP的发生、发展相关,早期密切观察血清HCY、TNF-α和IL-6水平变化对评估AP的严重程度和判断预后有一定的临床价值.     

不同类型冠心病患者血清炎症细胞因子水平比较

目的:分析炎症细胞因子在不同类型冠心病发生、发展过程中的作用并探讨其临床意义.方法:检测急性心肌梗死(AMI)组44例,不稳定型心绞痛(UAP)组44例,稳定型心绞痛(SAP)组43例及非冠心病患者(对照组)35例的血清白细胞介素(IL)-6、IL-8、IL-10和肿瘤坏死因子-α(TNF-α)浓度并进行比较.结果:与SAP组及对照组比较,AMI组和UAP组血清IL-6、IL-8、IL-10 、TNF-α水平均明显升高(P<0.01);AMI组血清IL-10、TNF-α水平高于UAP组(P<0.05),组间血清IL-6、IL-8水平差异无统计学意义(P>0.05);SAP组和对照组之间比较,血清IL-6、IL-8、IL-10、TNF-α水平均差异无统计学意义(P>0.05).结论:IL-6、IL-8、IL-10、TNF-α均参与了动脉粥样硬化斑块的形成和进展,血清细胞因子水平与冠心病病情严重程度密切相关.     

重症胰腺炎大鼠血清和胰腺组织Ang-Ⅱ、TNF-α、IL-10水平的变化

目的:探讨重症急性胰腺炎(SAP)大鼠血清和胰腺组织中血管紧张素Ⅱ(Ang-Ⅱ)、肿瘤坏死因子-α(TNF-α)、白细胞介素-10(IL-10)水平的动态变化及相关性。方法:64只健康雄性SD大鼠随机分为假手术组(SO组)和SAP组。利用ELISA法检测1、3、6、12 h血清、胰腺组织匀浆中TNF-α、Ang-Ⅱ、IL-10的水平。结果:SAP组血清、胰腺组织中Ang-Ⅱ水平较SO组明显升高(P0.05)。SAP组胰腺组织TNF-α水平明显升高,3 h达到高峰,而血清TNF-α水平1 h明显升高,6 h达高峰,与SO组比较,各时点差异具有统计学意义(P0.05)。SAP组胰腺组织IL-10水平各时点较SO组明显升高(P0.05);血清IL-10 3 h开始升高,12 h达高峰。结论:Ang-Ⅱ、TNF-α、IL-10在SAP大鼠胰腺组织及血清中平行产生,且均明显升高,表明Ang-Ⅱ参与胰腺炎过程,通过打破促/抗炎失衡,进而加重胰腺炎的炎症反应。     

不同类型的老年冠心病病人血清CRP与TNF-α、IL-6相关性研究

目的观察老年冠心病不同类型病人中肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)水平变化及其与C反应蛋白(CRP)之间的关系,进一步探讨老年急性冠状动脉综合征的临床预测的炎症指标.方法分别检测27例急性心肌梗死(AMI)病人(AMI组)、26例不稳定型心绞痛病人(UAP组)、52例稳定型心绞痛病人(SAP组),50名正常者(对照组).采用ELASA法测定血清TNF-α、IL-6浓度,免疫浊度分析法测定CRP的浓度.对比分析CRP与TNF-α、IL-6的相关性及各组间的差异.结果 AMI组及UAP组病人CRP、TNF-α和IL-6水平均显著高于对照组(P＜0.05)和SAP组(P＜0.05).AMI组与UAP组间血清CRP、TNF-α和IL-6比较均无统计学意义(P＞0.05),CRP水平与TNF-α、IL-6呈显著正相关(r=0.547,r=0.448,P＜0.01).结论细胞因子TNF-α、IL-6表达异常是促使急性冠状动脉综合征发生的主要机制之一.老年冠心病病人炎性标志物CRP与TNF-α、IL-6表达异常密切相关,可能是动脉粥样硬化斑块不稳定的标志.     

急性胰腺炎患者血清ICAM-1、TNF-α和P选择素浓度与病情严重程度的关系

目的研究急性胰腺炎患者血清ICAM-1、TNF-α和P选择素浓度和疾病严重程度的关系.方法选择重症急性胰腺炎(SAP)10例,轻症急性胰腺炎(MAP)10例,健康对照组10例,分别在患者入院后第1、3、5天抽取血清,检测血清中TNF-α、ICAM-1、P选择素水平.结果 SAP患者第1天ICAM-1,TNF-α,P选择素血清水平与MAP患者及对照组之间无显著性差异,而第3、5天SAP患者ICAM-1,TNF-α,P选择素血清水平与MAP患者及对照组之间均有显著性差异(P < 0.05).结论 ICAM-1、TNF-α、P选择素浓度升高与急性胰腺炎的严重程度有关.     

老年慢性支气管炎患者急性发作期血清肿瘤坏死因子-α、白细胞介素-6含量变化及对预后的影响

目的探讨老年慢性支气管炎患者急性发作期血清肿瘤坏死因子(TNF)-α、白细胞介素(IL)-6含量变化及对预后的判断价值。方法126例慢性支气管炎急性发作期患者按照慢性支气管炎的病情严重程度分为重症组和轻症组,观察两组急性发作期和缓解期的血清TNF-α、IL-6的含量变化及治疗后肺功能和肺啰音的改善情况。结果重症组急性发作期及缓解期血清TNF-α、IL-6的含量显著高于轻症组(P<0.05);重症组经治疗后肺功能及肺啰音的改善情况显著差于轻症组(P<0.05)。结论慢性支气管炎患者血清TNF-α、IL-6含量与患者病情严重程度呈显著相关性,且可作为预后的早期判断指标。     

低氧条件下 IL-6、IL-8、IL-10作用机制研究进展

低氧(hypoxia)是机体循环血液中氧分压较低的状态,缺氧则引发机体的一系列反应。随着研究的深入,发现机体内不但存在氧化应激反应,还伴随着一系列炎症反应,IL-6、IL-8、IL-10作为常见的炎症因子也成为研究热点,本文就低氧条件下三种 IL 的作用机制作一总结,为低氧造成的机体损伤提供更多理论依据,为低氧损伤的预防及治疗提供新靶点。     

Prognostic values of IL-6, IL-8, and IL-10 in acute pancreatitis

GOALS: The prognostic importance of interleukin-6 (IL-6), IL-8, and IL-10 in the prediction of acute pancreatitis severity. BACKGROUND: Early assessment of severity in acute pancreatitis could help the patients who are at risk of developing complications. Unfortunately, the used prognostic scoring systems generally are only moderately accurate in assessing disease severity. STUDY: We studied 117 consecutive patients with a diagnosis of acute pancreatitis admitted to our hospital during the past 2 years. Laboratory parameters and cytokines were analyzed from serum taken routinely on admission. Severity criteria were noted for each patient using Ranson, Glasgow, and APACHE II scoring systems. Local and systemic complications, developed during a follow-up period, were classified by Atlanta criteria. RESULTS: IL-6 was the only parameter that statistically significantly predicted complicated acute pancreatitis (P<0.05). IL-8 and IL-10 and the 3 prognostic scoring systems used did not properly assess complicated versus noncomplicated acute pancreatitis. CONCLUSIONS: Our prospective study supported the potential importance of IL-6 in the early assessment of complicated acute pancreatitis, but also suggested that pancreatitis classified as complicated in a large number of patients could not be correctly predicted with the Ranson, Glasgow, and APACHE II scoring systems.     

白细胞介素10基因转染对小鼠心脏移植排斥反应中细胞因子表达的影响

目的 :探讨白细胞介素 10 (IL 10 )基因转染对小鼠心脏移植排斥反应中IL 12、IL 15、IL 18和IL 4表达的影响。方法 :采用小鼠颈部心脏移植模型 ,随机分为 3组 :对照组、移植组和IL 10组。于术后第 5天取移植心脏 ,用逆转录聚合酶链式反应 (RT PCR)法观察IL 12、IL 15、IL 18、IL 4及IL 10的表达情况。结果 :移植组IL 12、IL 15、IL 18表达与对照组比较明显升高 ,IL 10、IL 4表达显著降低 (均P <0 .0 1)。IL 10组IL 12、IL 15、IL 18表达与移植组比较明显降低 ,而IL 4及IL 10表达显著升高 (均P <0 .0 1)。结论 :IL 10基因转染抑制心脏移植排斥反应主要与其抑制IL 12、IL 15、IL 18等Th1型细胞因子的表达 ,促进Th2型细胞因子IL 4的表达 ,使免疫反应由Th1型向Th2型偏移有关     

IL-12及IL-10在桥本甲状腺炎发病机制中作用的研究进展

桥本甲状腺炎是一种常见的慢性自身免疫性疾病,表现为辅助性T细胞(Th)1占优势。 Th1类细胞因子白细胞介素(IL)-12表达增加,在该病的诱发及慢性迁延中起重要作用,Th2类细胞因子IL-10表达的下调也与该病有关,且随病情变化二者表达水平有所不同。因此,这些细胞因子可作为病情变化的监测指标,并且可通过调节细胞因子的表达水平从而使失衡的Th1／Th2细胞趋于平衡。这可能为桥本甲状腺炎的治疗开拓一条新途径。     

急性冠脉综合征患者血清白介素6、8、10、18水平变化及其与冠状动脉病变程度的关系研究

目的观察急性冠脉综合征(ACS)患者血清白介素(IL)6、8、10、18水平变化,探讨其与冠状动脉病变程度的关系。方法选取2012年2月—2014年9月因非特异性胸部不适而在汕头市潮阳区大峰医院接受冠状动脉造影检查患者248例,根据造影结果分为ACS组159例、稳定性心绞痛组(SA组)47例、对照组42例,其中ACS组中急性心肌梗死(AMI)患者65例(AMI组),不稳定性心绞痛(UA)患者94例(UA组)。采用酶联免疫吸附试验(ELISA)检测各组受试者血清IL-6、IL-8、IL-10、IL-18水平,并分析其与ACS患者冠状病变程度的相关性。结果 AMI、UA、SA组患者血清IL-6、IL-8、IL-18水平高于对照组,AMI、UA组高于SA组,AMI组高于UA组(P0.05);AMI、UA组患者血清IL-10水平低于对照组和SA组,UA组低于AMI组(P0.05)。159例ACS患者中单支病变29例、双支病变56例、三支病变51例、多支病变23例,不同病变支数患者血清IL-6、IL-10、IL-18水平比较,差异无统计学意义(P0.05);单支病变、双支病变、三支病变患者血清IL-8水平低于多支病变患者,单支病变患者低于三支病变患者(P0.05)。159例ACS患者中,修正的Gensini积分等级G1级24例、G2级71例、G3级36例、G4级28例,G4级患者血清IL-6水平高于G1级患者(P0.05);G2、G3、G4级患者血清IL-8、IL-18水平高于G1级患者,G3、G4级患者高于G2级患者,G4级患者高于G3级患者(P0.05);G2、G3、G4级患者血清IL-10水平低于G1级患者,G3、G4级患者低于G2级患者,G4级患者低于G3级患者(P0.05)。Spearman相关分析结果显示,血清IL-18水平与冠状动脉病变支数呈正相关(r=0.196,P0.05),而血清IL-6(r=0.013)、IL-8(r=0.019)、IL-10(r=-0.014)水平与冠状动脉病变支数均无直线相关性(P0.05);线性相关分析结果显示,血清IL-18水平与修正的Gensini积分呈正相关(r=0.261,P0.05),而血清IL-6(r=0.028)、IL-8(r=0.039)、IL-10(r=-0.022)水平与修正的Gensini积分均无直线相关性(P0.05)。结论 ACS患者存在促炎/抗炎因子失衡,监测血清IL-18水平有助于判断ACS患者冠状动脉病变程度,而IL-6、IL-8、IL-10特异性较差。     

变应性鼻炎和哮喘患者血清IL-9、IL-4、IL-5变化及临床意义

目的探讨血清IL-9、IL-4、IL-5在变应性鼻炎、支气管哮喘（哮喘）、变应性鼻炎合并哮喘中的作用。方法采用双抗体夹心ELISA法检测哮喘组、过敏性鼻炎组、过敏性鼻炎合并哮喘（合并组）患者及查体健康者（对照组）的血清IL-9、IL-4、IL-5。结果与对照组比较,三组患者的血清IL-4、IL-5、IL-9均明显升高（P均〈0．01）;其中血清IL-5合并组高于哮喘组及过敏性鼻炎组（P〈0．01,〈0．05）,过敏性鼻炎组高于哮喘组（P〈0．01）;IL-4合并组高于哮喘组（P〈0．05）。结论IL-4、IL-5、IL-9参与过敏性鼻炎和哮喘的发病,三组患者均表现为Th2型细胞因子过度表达;变应性鼻炎合并哮喘的炎症程度较高,哮喘和鼻炎也有不同炎症反应。     

Serum IL-4, IL-10 and IL-6 levels in inflammatory arthritis

As the available in vitro and in vivo data suggest that interleukin (IL)-4 and IL-10 have immunosuppressive activity, our hypothesis was that serum IL-4 and IL-10 levels would correlate inversely with parameters of inflammation in patients with inflammatory arthritis. IL-4 was detected in the serum of 12 out of 140 patients with rheumatoid arthritis (RA), which was increased compared to the proportion found with patients with osteoarthritis (OA; P< 0.02). In addition, IL-4 was detected in the serum of 2 of 19 patients with systemic lupus erythematosus (SLE), 2 of 24 patients with psoriatic arthritis and 1 of 5 patients with Behçet's syndrome. No IL-4 was detected in patients with the following conditions: OA (58 patients), gout (17 patients), ankylosing spondylitis (6 patients), Reiter's syndrome (6 patients), polymyalgia rheumatica (6 patients), temporal arteritis (5 patients) and scleroderma (3 patients). No IL-10 was detected in any of the sera tested. We discuss the possible relevance of these results to the regulation of the immune response evident in inflammatory arthritis.     

DOWN-REGULATION OF FIBRINOGEN BIOSYNTHESIS BY IL-4, IL-10 AND IL-13

High levels of fibrinogen are recognized as an important vascular risk factor; however, it is not known if the increase of plasma fibrinogen is directly responsible for this risk, or is only a marker of vascular inflammation. To support this second hypothesis, Oncostatin M (OSM) is a potent stimulator of fibrinogen biosynthesis and induces smooth muscle cell proliferation. In the same way, we analysed whether interleukin-4 (IL-4), interleukin-10 (IL-10) or interleukin-13 (IL-13), which protect vessel walls from monocytes injuries leading to atherosclerosis, could influence fibrinogen biosynthesis. The two levels of regulation of fibrinogen biosynthesis were tested: firstly, the direct effect of these cytokines on fibrinogen production by the hepatoma cell line Hep G2, and secondly their effect on the secretion of hepatocyte stimulating factor (HSF) activity in the supernatant of lipopolysaccharide (LPS)-activated monocytes. IL-4 and IL-13 added to Hep G2 cells down-regulated both the increase of fibrinogen secretion induced by IL-6 and fibrinogen mRNA levels, this effect being more pronounced when Hep G2 were preincubated with the two cytokines before IL-6 addition. The effect of IL-10 was evidenced only on mRNA expression. IL-10 and IL-13 dose-dependently decrease HSF activity secreted by LPS-activated monocytes, whereas IL-4 had no effect. However, the three cytokines decreased HSF activity when monocytes were incubated with the cytokines before LPS activation. The effects of these cytokines on HSF activity are related to variations of IL-6 and OSM secretion. Our data strengthen the hypothesis that the fibrinogen level is a marker of vascular disease, since cytokines which have a protective vascular effect down-regulate fibrinogen production.     

Function of the interleukin-2 (IL-2) receptor gamma-chain in biologic responses of X-linked severe combined immunodeficient B cells to IL-2, IL-4, IL-13, and IL-15

The interleukin-2 (IL-2) receptor gamma-chain is a common component of several members of the cytokine receptor superfamily including those for IL-2, IL-4, IL-7, IL-9, IL-15, and possibly IL-13, and has recently been renamed the common gamma-chain (gamma c-chain). Transfection experiments have shown that the gamma c-chain participates in signal transduction by IL-2, IL-4 and IL-7, but a functional role for the gamma c-chain in biological responses by normal T cells and B cells to these cytokines has not been established. In this study, we have used X- linked severe combined immunodeficiency (X-SCID) as a naturally occurring gamma c-chain gene disruption model to examine the role of the gamma c-chain in human B-cell responses to IL-2, IL-4, IL-13, and IL-15. Our experiments show that B cells from two X-SCID patients with characterized gamma c-chain gene mutations do not respond to IL-2 or IL- 15, but respond as well or better than normal B cells to both IL-4 and IL-13 in assays for B-cell activation, proliferation, and IgE secretion. This finding raises important questions about the function of the gamma c-chain in receptors for IL-4 and IL-13, and the nature of the immune defect in X-SCID.