慢性肝病患者血清肿瘤坏死因子—α与白细胞介素—8水平关系的研究

用RIA法测94例慢性肝炎、肝硬化患者血清肿瘤坏死因子α(TNF-α)含量,同时用ELISA法测定其血清白细胞介素—8(IL—8)水平。结果表明慢性活动性肝炎和肝硬化患者血清中TNF-α明显高于对照组(P<0.01,P<0.05),且与其血清胆红素(BIL)和ALT呈正相关(P<0.05)。IL—8的阳性检出率及水平明显高于对照组(P<0.05～0.01),与其血清总胆红素(TB)亦呈正相关(P<0.05)。另外,患者血清TNF-α和IL—8定量明显相关(P<0.05)。提示TNF-α和IL—8参与了慢性肝脏炎症损害过程,并能反映病情活动程度,且TNF-α可能诱导IL—8的产生。     

乳癌患者血清TNF—α,IL—2表达水平及其临床意义

应用放免法检测了４０例乳癌，１０例乳腺良性疾病（下称良性组）患者及２０例正常者（下称对照组）的血清肿瘤坏死因子－α（ＴＮＦ－α）和白细胞介素－２（ＩＬ－２）的表达水平，结果显示，乳癌组术前血清ＴＮＦ－α水平明显高于对照组及良性组，术后２周乳癌组血清ＴＮＦ－α水平较术前明显降低，且各病期有显著性差异，有腋窝淋巴结转移（ＬＮ＾＋）者高于无腋窝淋巴结转移（ＬＮ＾－）者，提示测定术后ＴＮＦ－α表达水平，对     

伴骨髓水肿的膝骨关节炎患者白细胞介素-1β白细胞介素-6肿瘤坏死因子-α的相关性研究

目的 探讨血清及关节液白细胞介素(IL)-1β,IL-6,肿瘤坏死因子(TNF)-α与伴有骨髓水肿的膝骨关节炎(KOA)的相关性.方法 收集我院KOA患者331例,根据膝关节磁共振成像(MRI)分为骨髓水肿组(172例)和非骨髓水肿组(159例),分别收集其临床症状、骨关节指数( WOMAC)评分,并同期检测其血清和关节液中IL-1β,IL-6,TNF-α水平,采用单因素方差分析比较2组之间的差异,Spearman相关分析探讨其炎症指标水平与骨髓水肿发生程度及其临床指标的相关性.结果 ①KOA患者血清及关节液IL-1β、IL-6,TNF-α表达水平均呈正相关(血清r=0.24,0.38;关节液r=0.20,0.29;P均＜0.05);IL-6与TNF-α水平呈正相关(血清r=0.31,P＜0.05;关节液r=0.33,P＜0.05).②KOA伴骨髓水肿组内,血清及关节液IL-6和TNF-α水平较KOA不伴骨髓水肿组高(血清F=8.139,7.172;关节液F=9.201,7.001,P均＜0.05);③血清及关节液IL-6,TNF-α水平与KOA伴发骨髓水肿容积积分(血清rs=0.27,0.26;关节液rs=0.29,0.32;P均＜0.05)和程度积分(血清r,=0.29,0.27;关节液r,=0.29,0.31;P均＜0.05)呈正相关;④血清及关节液IL-1β,IL-6,TNF-α在伴有滑膜炎组的KOA中明显升高(骨髓水肿组血清F=3.931,5.866,5.514;关节液F=4.211,5.202,5.972;P均＜0.05.非骨髓水肿组血清F=3.513,3.114,7.112;关节液F=3.722,3.965,8.891;P均＜0.05).结论 IL-1β,IL-α,TNF-α在KOA伴有滑膜炎时明显升高,在KOA伴骨髓水肿时尤以IL-6,TNF-α升高明显.     

急性脑梗死患者血清白细胞介素-10含量的变化及意义

近年来，急性脑梗化后脑损伤的病理生理学研究进展很快，主要集中在缺血后的炎症过程。白细胞介素（IL）-1和肿瘤坏死因子（TNF）-α被认为是主要介质，与干扰素（IF）-γ、IL-6、1L-8和生长因子一起启动脑组织局部的炎症反应，关于抗炎因子IL-10在改善缺血周围脑组织血液供应及如何减轻致炎因子作用方面，     

慢性肝病患者血清TNFα、IL-1和IL-8测定及临床意义

本研究通过对 98例各型慢性肝病患者血清肿瘤坏死因子α(TNFα)、白细胞介素 1(IL 1)和白细胞介素 8(IL 8)水平的检测 ,探讨其在慢性肝病发生发展中的作用及临床意义。材料与方法一、研究对象98例慢性肝病患者均为本院感染科住院及门诊病例。其中慢性肝炎轻度 19例 ,男 13例 ,女 6例 ,年龄 2 3～ 61岁 ,平均3 9 .5岁 ;慢性肝炎中重度 2 5例 ,男 17例 ,女 8例 ,年龄 2 7～ 66岁 ,平均 3 8.8岁 ;慢性重型肝炎 2 9例 ,男 2 0例 ,女 9例 ,年龄 2 5～ 64岁 ,平均 3 9.7岁 ;肝炎后肝硬化 (肝硬化 ) 2 5例 ,男 16例 ,女 9例 ,年龄 2 8～ 69岁 …     

脑梗死患者血清TNF-α、IL-6含量的变化及意义

本研究旨在通过检测老年动脉硬化性脑梗死患者急性期和恢复期血清肿瘤坏死因子-α(TNF-α)、白细胞介素6(IL-6)含量变化,探讨检测细胞因子在脑梗死发展过程中的价值及意义,为临床防治提供理论依据。1资料与方法1.1一般资料66例均为我院神经内科住院急性脑梗死(ACI)患者,男40例,     

胃癌患者血清TNF—α、IL-6、IL-8水平变化及意义

目的观察胃癌患者血清肿瘤坏死因子-α（TNF-α）、IL-6、IL-8的水平变化,并探讨其临床意义。方法采用ELISA法测定60例胃癌（胃癌组）、25例胃良性病变患者（良性组）血清TNF-α、IL-6、IL-8,并与25例健康者（正常组）作对照。结果胃癌组血清TNF-α、IL-6、IL-8水平明显高于良性组和正常组（P〈0．05）,且TNF—α、IL-6、IL-8水平随着胃癌临床病理分期的增加而升高（P〈0．05）。肿瘤根治手术后患者血清TNF—α、IL-6、IL-8水平较术前明显降低（P〈0．05）;良性组血清TNF—α、IL-6、IL-8水平与正常组近似（P〉0．05）。结论胃癌患者血清TNF—α、IL-6、IL-8水平增高;检测胃癌患者血清TNF—α、IL-6、IL-8有助于病情判断和估计预后。     

白细胞介素8和肿瘤坏死因子α与哮喘病情

白细胞介素８和肿瘤坏死因子α与哮喘病情吴伟王新力呼吸道炎症介质产生、释放常常成为促发哮喘发作和加剧病情的主要因素，其中白细胞介素８（ＩＬ－８）和肿瘤坏死因子α（ＴＮＦ－α）是前炎症反应因子（ＰＩＣ），它们在炎症反应中起重要作用。为此我们探讨两者在哮喘...     

重型肝炎患者血清肿瘤坏死因子α与白细胞介素10和15水平的研究

重型肝炎肝细胞损伤的病理机制与机体的免疫应答和免疫调节紊乱密切相关。细胞因子是一类由免疫活性细胞产生的小分子多肽或蛋白质,其异常分泌和生成能引起机体许多病理性紊乱,细胞因子在病毒性肝炎发病机制中的作用愈来愈被重视,我们应用ELISA法检测了重型乙型肝炎患者血清TNFα,IL-10及IL-15水平,探讨它们在重型肝炎免疫发病机制中的意义。一、资料与方法1.对象:1999年3月-2004年2月我院感染内科住院     

伤寒患者血清可溶性白细胞介素—2受体和肿瘤坏死因子水平变化

伤寒患者血清可溶性白细胞介素２受体和肿瘤坏死因子水平变化沈燕关磊晶熊金凤王成勇本试验动态观察了伤寒患者不同病期中血清可溶性白细胞介素２受体（ｓＩＬ２Ｒ）和肿瘤坏死因子（ＴＮＦ）水平的变化，以探讨二者在伤寒发病机制中所起的作用。现将结果报道如下。...     

老龄大鼠脑缺血肝脏前列腺素和肿瘤坏死因子的变化

目的：从血栓素A2（TXA2）与前列环素（PGI2）平衡失调和肿瘤坏死因子（TNF）方面研究老龄大鼠脑缺血再灌注肝脏损伤机制。方法：青年（5月龄）和老龄（20月龄以上）大鼠均分为模型组和对照组,观察大鼠全脑缺血30min再灌注60min后肝脏组织形态和胆红素、丙二醛（MDA）、血栓素B2（TXB2）、6－酮－前列腺素F1α（6-Keto-PGF1α）含量及丙氨酸氨基转移酶（ALT）、天门冬氨酸氨基转移酶（AST）的活性的变化。结果：青年和老龄 模型组大鼠肝脏组织形态和功能均出现明显的病理改变,老龄模型组较青年模型组严重。老龄对且和青年模型肝组织TXB2／6－Keto-PGF1α高于青年对照组,老龄模型组高于老龄对照组,青年模型组和老龄模型组肝脏TNF高于青年对照组和老龄对照组。结论：脑缺血再灌注肝脏损伤老龄大鼠青年大鼠严重,TXA2与PGI2平均失调和TNF介导的作用可能参与肝脏损伤。     

Levels of TNF,TNF autoantibodies and soluble TNF receptors in patients with bronchial asthma

Abstract

Objectives: The aim of the study was to evaluate the potential contribution made by tumor necrosis factor (TNF) autoantibodies to the pathogenesis of bronchial asthma (BA). Methods: We used affinity chromatography methods and a magnetic separation procedure to purify human autoantibodies specific to TNF. The autoantibodies were used as a calibration material to determine the absolute content of autoantibodies to TNF using enzyme-linked immunosorbent assay (ELISA). TNF content and levels of soluble receptors to TNF were determined using the ELISA commercial test kits. Results: We demonstrated significant increases in the levels of TNF and soluble TNF receptors in the sera of patients with uncontrolled and controlled BA, as compared with healthy donors. Levels of autoantibodies of the IgG2 and IgG4 subclasses were significantly higher in sera from patients with uncontrolled BA than in healthy donors. Levels of IgG2 autoantibodies were significantly higher in sera from patients with uncontrolled BA than in patients with controlled BA. Conclusions: BA is associated with changes in the levels of not only TNF and soluble receptors for TNF, but also autoantibodies to TNF. Given the magnitude of the changes in the levels of different subclasses of autoantibodies to TNF, we propose that these autoantibodies might contribute to the pathogenesis of BA.     

支原体肺炎肺外损伤患儿T细胞亚群、IFNγ、TNFα的变化及意义

目的 探讨支原体肺炎肺外损伤患儿细胞免疫、细胞因子状况和胸腺肽的治疗效果。方法 采用流式细胞仪和酶标仪检测31例支原体肺炎肺外损伤组患儿急性期、恢复期血中CD3CD4、CD8、CD4／CD8干扰素γ（IFNγ）、肿瘤坏死因子α（TNFα水平，并与支原体肺炎组比较。结果 ①急性期支原体肺炎肺外损伤组和支原体肺炎组比较，CD3、CD4显著降低（P〈0．05），TNFα显著升高（P〈0．01），CD8、IFNγ无统计学意义（P〉0．05）；②支原体肺炎肺外损伤组急性期和4周后比较，CD3、CD4、IFNγ升高（P〈0．05），TNFα显著降低（P〈0．01），CD8无变化。用胸腺肽治疗患者以上指标变化更明显。结论 支原体肺炎肺外损伤患儿细胞免疫功能低于支原体肺炎患儿；细胞因子中TNFα早期升高，而IFNγ不明显；恢复期TNFα下降，而IFNγ升高明显。用胸腺肽治疗能缩短病程。     

TNF and sepsis

Recent experiments have demonstrated that TNF plays an important role in the pathogenesis of septic shock. To confirm the involvement of TNF in human septic shock, serum TNF levels were measured in 10 adult patients admitted to the intensive care unit for sepsis with or without shock. Septic shock was corroborated by hemodynamic data (right catheterization, measurement of cardiac output by thermodilution). For TNF measurement, venous blood samples were withdrawn, as soon as possible after the onset of sepsis, into a pyrogen--free tube. Serum TNF levels were determined using a radioimmunoenzymatic assay (IRE Medgenix). During septic shock (n = 7), TNF levels were significantly higher (m = 354 +/- 131 pg/ml) than during sepsis without shock (n = 8; m = 145 +/- 35 pg/ml) (p less than 0.0005). TNF levels were also significantly higher in non-survivors (m = 392 +/- 111 pg/ml) than in survivors (m = 167 +/- 81 pg/ml) (p less than 0.0005). The value of 250 pg/ml seems to be critical: no patient without shock had TNF levels above 250 and all the patients who died early during the first 24 h) had TNF levels above 250. The TNF level is negatively correlated with the platelet count (r = -0.70; p less than 0.05). These data favor a pathophysiological for TNF in human sepsis and septic shock.     

Circulating levels of TNF alpha and TNF receptor superfamily members in lymphoid neoplasia

We have correlated the serum levels of TNF alpha and soluble TNF receptor superfamily members with clinico-pathologic parameters in patients of Hodgkin's disease (HD, N = 26) and non-Hodgkin's lymphoma (NHLs, N = 35). HD patients had significantly higher levels of TNF alpha, sTNFRI, and sTNFRII in serum while NHL patients had significantly higher levels of sTNFRI, sTNFRII, sCD27, and sFas as compared to controls. In NHL patients the levels of sCD27 correlated directly and significantly with the high-stage disease, bone marrow involvement, lymph nodal presentation, and serum LDH levels. Similarly in NHL patients, levels of sFas also correlated directly and significantly with the presence of high stage disease. HD patients with B symptoms had significantly higher levels of sTNFRII.     

Requirement of TNF and TNF receptor type 2 for LPS-induced protection from lethal septic peritonitis

Pretreatment of mice with low quantities of LPS induces endotoxin tolerance characterized by enhanced resistance to lethal doses of LPS and to a number of infectious challenges. Mice subjected to cecal ligation and puncture (CLP) survived the ensuing septic peritonitis significantly better when they had been pretreated with LPS. This LPS-induced protection was dependent on endogenous TNF production capacity since LPS pretreatment did not protect TNF-deficient mice from death after CLP. While mice deficient in the TNF receptor type 2 (p75TNFR) were as sensitive to CLP-induced mortality as control mice, LPS pretreatment could not reduce mortality in p75TNFR-deficient mice after CLP. Therefore, activation of the TNF receptor type 2 by endogenous TNF constitutes an important interaction for the development of LPS-induced resistance to bacterial infection.     

TNF alpha and heart failure

Tumor necrosis factor alpha (TNF alpha) is a cytokine with proinflammatory properties which produces negative inotropic effects on the heart. It is produced in a variety of conditions such as septic shock, acute myocarditis, reperfusion injury, and congestive hear failure (CHF). This production is probably due to activation of immune elements localized in the heart or periphery, or both. TNF alpha acts by binding to two specific receptors: TNF-R1 and TNF-R2. These two proteins have different effects. TNF-R1 has cytotoxic and antiviral activity, induces fibroblast proliferation, and mediates apoptosis. TNF-R2 is involved in septic shock and in lymphocyte proliferation. They both have negative inotropic effect on the heart. It has been showed that these receptors are down-regulated in congestive heart failure, while their soluble forms (sTNF-R1 and sTNF-R2) increase with the severity of symptoms. However the significance of this increase is still unclear. The role of Fas, a receptor protein that induces apoptosis, is also examined. Fas and its ligand have homologies respectively with TNF alpha and TNF-R. Also the soluble form of Fas (sFas) increases in relation to heart failure and is related to soluble forms of the similar receptor family, therefore it is possible that the same stimuli lead the three receptors to act together. SFas, as well as sTNF receptors, may play an important role in CHF.     

Selective death of autoreactive T cells in human diabetes by TNF or TNF receptor 2 agonism

Human autoimmune (AI) diseases are difficult to treat, because immunosuppressive drugs are nonspecific, produce high levels of adverse effects, and are not based on mechanistic understanding of disease. Destroying the rare autoreactive T lymphocytes causing AI diseases would improve treatment. In animal models, TNF selectively kills autoreactive T cells, thereby hampering disease onset or progression. Here, we seek to determine, in fresh human blood, whether TNF or agonists of TNF selectively kill autoreactive T cells, while sparing normal T cells. We isolated highly pure CD4 or CD8 T cells from patients with type 1 diabetes (n = 675), other AI diseases, and healthy controls (n = 512). Using two cell death assays, we found that a subpopulation of CD8, but not CD4, T cells in patients' blood was vulnerable to TNF or TNF agonist-induced death. One agonist for the TNFR2 receptor exhibited a dose-response pattern of killing. In type 1 diabetes, the subpopulation of T cells susceptible to TNF or TNFR2 agonist-induced death was traced specifically to autoreactive T cells to insulin, a known autoantigen. Other activated and memory T cell populations were resistant to TNF-triggered death. This study shows that autoreactive T cells, although rare, can be selectively destroyed in isolated human blood. TNF and a TNFR2 agonist may offer highly targeted therapies, with the latter likely to be less systemically toxic.