Effects of n-3 fatty acids on serum interleukin-6, tumour necrosis factor-alpha and soluble tumour necrosis factor receptor p55 in active rheumatoid arthritis

We investigated the effects of a low n-6 fatty acid (FA) diet supplemented with fish oil on serum pro-inflammatory cytokine concentrations and clinical variables in patients with active rheumatoid arthritis (RA). Sixty patients were randomly assigned to receive a diet low in n-6 FAs and n-3 FAs supplement (fish oil group), a diet low in n-6 FAs and placebo (placebo group), or no special diet or intervention (control group). Serum cytokines and clinical and biochemical variables were evaluated at baseline and various timepoints. At week 18 the fish oil group had significant reductions in linoleic acid, C-reactive protein (CRP) and soluble tumour necrosis factor receptor p55 (sTNF-R p55), and significant elevations in eicosapentaenoic acid and docosahexaenoic acid compared with baseline. There were no significant differences in the clinical variables between the three groups. At week 24 there were significant reductions in interleukin-6 and TNF-alpha in the fish oil and placebo groups. Supplementation with n-3 FA and a low n-6 FA intake decreased serum sTNF-R p55 and CRP levels in patients with RA.     

Circulating interleukin-6, tumour necrosis factor soluble receptor-II,interleukin-1 receptor antagonist,and serum procalcitonin in patients with heat stroke: Prognostic implications

Heat Stroke (HS) is frequently fatal illness that usually occurs episodically as clusters of patients presenting to the emergency room. We have studied 26 patients with HS incurred during the religious pilgrimage to Makkah at (0, 6, 12, 24 hr) and found that the level of IL-Ira, TNF SR II and IL-6 are elevated. It appears such elevation are required for and are part of acute phase response and recovery. However markedly elevated cytokines are associated with mortality. We also found the precursors to the hormone calcitonin: Procalcitonin are greatly increased in patients with this condition. Although serum levels are high upon admission (3.4±1.0 ng/ml vs 0.17±0.04 ng/ml for a febrile emergency room control (P=0.012), even higher levels occured at 6 hours 25.1±6.4 ng/ml, (P<0.0001). Among the 6 patients who died 4 of them had levels indistinguishable from control subjects, the other 2 patients who had high levels, had additional medical complications. Chi-square analysis of categorized Pro CT revealed a significant positive correlation between Pro CT and survival. Our study shows that the level of IL-Ira, TNF SR II and IL-6 are increased in HS and associated with mortality and also it may suggest that the hyperprocalcitoninemia may be related to the post-injury cytokine cascade. The mechanism by which hyperprocalcitoninemic response is elicited in surviving HS patients, but fail to occur in most of those who do not survive requires further study.     

急性肺损伤兔肺泡灌洗液及血清肿瘤坏死因子α、白细胞介素1β和白细胞介素6浓度变化与小剂量高渗盐水的干预

目的:观察创伤性休克兔经小剂量高渗盐水治疗后肺部炎症反应及病理学损伤的变化情况,进一步研究高渗盐水对创伤应激状态下急性肺损伤的作用及其机制。方法:实验于2005-08/2006-04在华中科技大学同济医学院附属同济医院急诊科实验室完成。①实验分组:新西兰白兔30只随机分为3组:假手术组、生理盐水处理组、高渗盐水治疗组,每组10只。②实验方法:假手术组:局部麻醉下行插管术及肝素化,静脉输注平衡盐80mL。生理盐水处理组:用骨钳致兔一侧股骨中下1/3粉碎性骨折,经股动脉放血至储血瓶内,使平均动脉压降至(40±5)mmHg,45min后输注生理盐水4mL/kg,再回输储血及2倍于失血量的平衡盐液进行复苏。高渗盐水治疗组:除以75g/L的氯化钠溶液代替生理盐水外,其余处理同生理盐水处理组。在休克前、休克末、复苏后2h、4h分别采集静脉血1mL备用。复苏后4h空气栓塞处死动物,进行支气管肺泡灌洗,收集支气管肺泡灌洗液。③评估指标:双抗体夹心ELISA法测定支气管肺泡灌洗液以及血清肿瘤坏死因子α、白细胞介素1β、白细胞介素6的浓度;凝胶电泳迁移率改变分析法检测肺泡巨噬细胞核蛋白提取物中核因子κB的活性;显微镜观察肺组织的病理改变。结果:30只实验动物均进入结果分析。①血清细胞因子浓度的变化:与假手术组比较,生理盐水处理组肿瘤坏死因子α浓度在休克发生后迅速升高(P<0.05),复苏后又进一步上升(P<0.01),白细胞介素1β及白细胞介素6浓度在复苏后4h才有明显增加(P<0.01)。高渗盐水治疗组与生理盐水处理组比较,复苏后2～4h肿瘤坏死因子α、白细胞介素1β及白细胞介素6浓度均有不同程度下降(P<0.05,P<0.01,P<0.05)。②支气管肺泡灌洗液细胞因子浓度的变化:生理盐水处理组肿瘤坏死因子α、白细胞介素1β及白细胞介素6浓度均显著高于假手术组(P均<0.01),高渗盐水治疗组各细胞因子的浓度虽然也高于假手术组(P<0.05,P<0.01,P<0.01),但与生理盐水处理组比较均有明显降低(P<0.05,P<0.01,P<0.01)。③肺泡巨噬细胞核因子κB的活性变化:生理盐水处理组核因子κB的活性远高于假手术组(P<0.01),而高渗盐水治疗组核因子κB的活性虽然也高于假手术组(P<0.01),但与生理盐水处理组比较有显著降低(P<0.01)。④肺组织病理学改变:高渗盐水治疗组肺水肿及炎性细胞浸润明显减轻;Ⅰ、Ⅱ型肺泡上皮细胞内仅有少量空泡,上皮基本完整,基底膜增厚不明显。结论:小剂量高渗盐水治疗可抑制创伤性休克时核因子κB的活化,减少促炎细胞因子的合成与分泌,减轻肺部的炎症反应,从而发挥对急性肺损伤的保护作用。     

Pharmacokinetic-pharmacodynamic modeling of the inhibitory effect of erythromycin on tumour necrosis factor-alpha and interleukin-6 production

Erythromycin inhibits the production of tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL6) induced by heat-killed Streptococcus pneumoniae in human whole blood ex-vivo. The objective of the present study was to determine and characterize the concentration-effect relationship of this phenomenon in order to predict its possible clinical relevance.Six healthy volunteers received a single intravenous dose of 1000 mg erythromycin. Blood samples were obtained up to 4 h after drug administration. Samples were assayed for erythromycin concentrations and (after heat-killed Streptococcus pneumoniae stimulation) for TNF-alpha and IL6 concentrations. Effect vs. time data from individual subjects were fitted to the indirect response model with an Emax concentration-effect relationship. Simulations of these effects were performed for therapeutic intravenous and oral erythromycin dosage regimens. The geometric means of the values of Kin, Kout and EC50 were 15.4 microg/h, 0.82/h, 9.4 mg/L for TNF-alpha and 321 microg/h, 2.02/h, 18.3 mg/L for IL6. Simulations revealed a maximal inhibition of TNF-alpha concentrations of 35%, 50%, 16% and 27% at erythromycin dosages of 500 mg i.v., 1000 mg i.v., 500 mg p.o and 1000 mg p.o. q 6 h, respectively, whereas a maximal inhibition of IL6 of 29%, 44%, 13% and 22% are predicted for the respective regimens. The inhibitory effect of erythromycin on TNF-alpha and IL6 production can be adequately described by the indirect response model with an Emax concentration-effect relationship. Simulations predicted a substantial decrease of production of these cytokines at intravenous and to a much lesser extent at oral erythromycin dosage regimens.     

C-reactive protein, fibrinogen, interleukin-6 and tumour necrosis factor-alpha in the prognostic classification of unstable angina pectoris

BACKGROUND: Inflammatory process has been found to play an important role in the pathogenesis of coronary heart disease (CHD) and in the prognosis of CHD patients. AIM. The aim of this study was to investigate the prognostic value of C-reactive protein (CRP), fibrinogen, interleukin (IL)-6 and tumour necrosis factor-alpha (TNF-alpha) in patients with unstable angina pectoris (UAP), including factor analysis to assess their joint effects. METHODS: The study comprised 263 consecutive patients (159 men, 104 women; median age 68 years) with UAP. Blood samples for the acute-phase protein and cytokine determinations were drawn on admission. RESULTS: Coronary mortality during the median follow-up time of 17 months was 6-fold higher in the highest tertile for CRP and IL-6 and 3.5-fold higher in the highest tertile for fibrinogen and TNF-alpha than in the respective combined lower tertiles. Factor analysis produced two underlying factors, ie the 'inflammation' factor, including CRP, fibrinogen and IL-6, and the 'injury' factor, including troponin T, creatine kinase MB mass and TNF-alpha. In Cox models, both of these factors were independent predictors of the risk of coronary death and major coronary events (coronary death or nonfatal myocardial infarction). CONCLUSIONS: Elevated levels of acute-phase proteins and cytokines, particularly CRP and IL-6, are strong predictors of the risk of serious coronary events in patients with UAP.     

Interleukin-6 but not tumour necrosis factor-alpha predicts survival in patients with advanced cancer

Purpose

The purpose of this study was to evaluate the prognostic role of interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-α) in the survival of patients with advanced cancer.

Methods

In this prospective cohort study between three hospice and palliative care centres in South Korea, we followed 98 advanced cancer patients until death or the end of the study. Approximately 60 % of the patients had poor functional status (Eastern Cooperative Oncology Group score ≥3). We investigated the symptoms of cancer cachexia anorexia syndrome, possible cytokine-related confounders such as infection and medication records. Influence from clinical variables was adjusted using the Cox proportional hazard model.

Results

The median survival time was 27 days. On multivariate analysis, elevated IL-6 (hazard ratio, 2.139; p?=?0.003) was found to be an independent significant prognostic factor. TNF-α was not a significant factor. Poor performance status and male gender were also independently related to shortened survival.

Conclusions

IL-6 level can be a useful indicator of survival time of patients with advanced cancer at the very end of life. In contrast, the prognostic role of TNF-α requires further study.     

Cerebrospinal fluid tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, and interleukin-8 as diagnostic markers of cerebrospinal fluid infection in neurosurgical patients

OBJECTIVE: To evaluate whether cerebrospinal fluid concentrations of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, or IL-8 may be used as diagnostic markers for the differential diagnosis of aseptic vs. bacterial meningitis and/or ventriculitis in neurosurgical patients. DESIGN: Prospective, observational study. SETTING: University teaching hospital. SUBJECTS: A total of 112 cerebrospinal fluid samples from 14 asymptomatic patients with normal cerebrospinal fluid after neurosurgery, 27 asymptomatic and 19 symptomatic patients with postneurosurgical aseptic meningitis, 32 patients with postneurosurgical cerebrospinal fluid infection, and 20 with severe subarachnoid and/or cerebral hemorrhage. MEASUREMENTS AND MAIN RESULTS: Specific ELISA kits were used to analyze TNF-alpha, IL-1beta, IL-6, and IL-8 concentrations on cerebrospinal fluid samples. Elevations in cerebrospinal fluid concentrations of TNF-alpha, IL-1beta, IL-6, and IL-8 were induced by different diseases or neurosurgical procedures, but cerebrospinal fluid bacterial infection induced the highest concentrations. To discriminate between aseptic cerebrospinal fluid pleocytosis and cerebrospinal fluid infection with a specificity of 95%, cerebrospinal fluid leukocyte count >1700/mL, TNF-alpha >150 pg/mL, and IL-1beta >90 pg/mL showed sensitivities of 51%, 74%, and 90%, respectively. Sufficiently sensitive and specific cutoff points could not be found for cerebrospinal fluid IL-6 or IL-8. CONCLUSION: Cerebrospinal fluid IL-1beta appears to be the best biochemical marker of cerebrospinal fluid infection in neurosurgical patients.     

TGF-β1、TNF-α、IL-6与多囊卵巢综合征发病关系的探讨

目的：探讨TGF-β1、TNF-α、IL-6与多囊卵巢综合征(PCOS)发病的关系。方法：酶联免疫吸附试验(EusA)检测血清TGF-β1、TNF-α、IL-6水平，放射免疫法(RIA)检测血清胰岛素水平，葡萄糖氧化酶法检测血糖水平，化学发光仪检测血清甾体激素水平。结果：(1)TGF-β1水平在PCOS组高于对照组，在两组中与其他指标均无相关性；TNF-α水平在PCOS组明显高于对照组，且与IL-6水平呈明显正相关，与胰岛素敏感指数(ISI)呈明显负相关，与睾酮(T)和雄烯二酮(A2)呈正相关，在两组中均与BMI呈正相关；IL-6水平在PCOS组明显高于对照组，且与BMI呈正相关，与空腹胰岛素(FIN)水平呈明显正相关，与ISI呈明显负相关，对照组中与各项指标无相关性。（2）PCOS组有IR者TNF-α、IL-6、FIN明显高于无IR者。结论：TGF-β1、TNF-α、IL-6都与PCOS的发病有关，TGF-β1可能主要影响胰岛素的敏感性和糖代谢，TNF-α、可能主要通过影响外周组织对胰岛素的敏感性和导致局部雄激素水平升高来发挥作用，IL-6主要与IR有关，TNF-α和IL-6有协同作用，能加重PCOS病情的发生发展。     

Vascular and fibrinolytic effects of intra-arterial tumour necrosis factor-alpha in patients with coronary heart disease

Elevated plasma t-PA (tissue plasminogen activator) and serum CRP (C-reactive protein) concentrations are associated with an adverse cardiovascular risk. In the present study, we investigated whether acute local inflammation causes vascular dysfunction and influences t-PA release in patients with stable coronary heart disease. Serum CRP, plasma t-PA and PAI-1 (plasminogen activator inhibitor type 1) concentrations were determined in 95 patients with stable coronary heart disease. A representative subpopulation of 12 male patients received an intra-brachial infusion of TNF-alpha (tumour necrosis factor-alpha) and saline placebo using a randomized double-blind cross-over study design. Forearm blood flow and plasma fibrinolytic and inflammatory variables were measured. Serum CRP concentrations correlated with plasma t-PA concentrations (r=0.37, P<0.001) and t-PA/PAI-1 ratio (r=-0.21, P<0.05). Intra-arterial TNF-alpha caused a rise in t-PA concentrations (P<0.001) without affecting blood flow or PAI-1 concentrations. TNF-alpha pretreatment impaired acetylcholine- and sodium nitroprusside-induced vasodilatation (P<0.001 for both) whilst doubling bradykinin-induced t-PA release (P=0.006). In patients with stable coronary heart disease, plasma fibrinolytic factors correlate with a systemic inflammatory marker and local vascular inflammation directly impairs vasomotor function whilst enhancing endothelial t-PA release. We suggest that the adverse prognosis associated with elevated plasma t-PA concentrations relates to the underlying causative association with vascular inflammation and injury.     

Biological variation of interleukin-1beta, interleukin-8 and tumor necrosis factor-alpha in serum of healthy individuals.

Components of biological variation can be used to assess the usefulness of reference values, to evaluate the significance of changes in serial results from an individual and to define objective analytical goals. The aim of the study was to assess, in 15 healthy subjects studied at regular monthly intervals over a period of 6 consecutive months, the biological variation of interleukin-1beta (IL-1beta), interleukin-8 (IL-8), and tumor necrosis factor-alpha (TNF-alpha). Biological variation data (within-subject and between-subject coefficient of variation (CV)) were determined using a simple nested analysis of variance. Derived parameters (index of individuality, reliability coefficient and critical diferences) were calculated from within-subject and between-subject CV. The mean and standard deviation (SD), within-subject CV, between-subject CV, index of individuality and reliability coefficient were as follows: for IL-1beta, 0.67 (0.32) pg/ml, 30%, 36%, 0.85, and 0.76; for IL-8, 3.68 (1.45) pg/ml, 24%, 31%, 0.85 and 0.75; and for TNF-alpha, 3.14 (1.87) pg/ml, 43%, 29%, 1.56 and 0.50, respectively. We conclude that between-subject variation and within-subject variation are quite similar for IL-1beta and IL-8 and are relatively high for the three cytokines studied. Index of individuality is less than 1.4 for IL-1beta and IL-8, and thus reference intervals based on population studies are of limited value. On the contrary, the index of individuality for TNF-alpha is greater than 1.4 and reference values can be used for diagnosis. Quality goals for imprecision are easily achieved for the three cytokines with current methodology.     

阻塞性睡眠呼吸暂停患者循环内皮细胞与血清肿瘤坏死因子-α、白介素-6浓度的关系

目的:探讨阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者循环内皮细胞(CECs)数量及凋亡与血清致炎因子肿瘤坏死因子-α(TNF-α)、白介素-6(IL-6)浓度之间的关系.方法:将研究对象分为对照组、轻度OSAHs组、中度OSAHs组和重度OSAHS组(各12例),所有对象于夜间行多导睡眠图仪检查,次晨采外周静脉血,流式细胞仪检CECs的数量和凋亡情况,ELISA检测血清TNF-α、IL-6浓度.结果:CECs数量及凋亡率在重度和中度OSAHS组皆较对照组和轻度组升高(P<0.05);血清TNF-α浓度在重度和中度组皆较对照组和轻度组升高(P<0.05),血清IL-6浓度在各组对象之间差异无显著性(P>0.05);外周静脉血CECs数量与OSAHS患者AHI成正相关(r=0.849,P<0.001);CECs凋亡率与AHI成正相关(r=0.462,P=0.001),与血清TNF-α浓度成正相关(r=0.555,P<0.001),与夜间最低血氧饱和度(LsaO2)成负相关(r=-0.481,P=0.001),与血清IL-6浓度无相关关系(P=0.186).结论:OSAHS患者可能通过分泌TNF-α,在血管内皮细胞损伤过程中发挥毒性作用,并与病情严重程度、夜间缺氧密切相关.     

Circulating interleukin-1 beta and tumor necrosis factor-alpha concentrations after burn injury in humans.

OBJECTIVES: To measure plasma interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF alpha) concentrations after burn injury and to determine if these concentrations relate to clinical status. DESIGN: Prospective assessment. SETTING: Hospital burn unit. PATIENTS: Thirty-one patients with second- or third-degree burns, covering 10% to 95% of body surface area. MEASUREMENTS AND MAIN RESULTS: Initial concentrations of IL-1 beta were increased (mean 188 +/- 31 pg/mL), and the concentrations for each patient correlated with body temperature at the time of the blood sample (rho = 0.51, p < .015) (rho is a nonparametric statistical measure; a nonparametric analysis is mandatory for data that is categorical [Acute Physiology and Chronic Health Evaluation, APACHE, scores] and data that are not normally distributed [IL-1 beta and tumor necrosis factor, TNF, data]). Mean TNF alpha concentrations were initially 264 +/- 132 pg/mL, and these concentrations were positively related to body temperature (rho = 0.41, p < .05) and inversely related to the total WBC count (rho = -0.45, p < .025). Through the course of hospitalization, plasma cytokine levels fluctuated, but transient increases (sometimes into the nanogram/mL range) did not consistently correspond to changes in clinical signs or severity of illness, as determined by APACHE II scores. The maximum plasma cytokine levels in any patient were not related to age, but maximum IL-1 beta concentrations were inversely related to burn size (rho = -0.46, p < .015). The final IL-1 beta concentrations measured in the patients who died (n = 7) were significantly less than measurements in surviving patients matched for burn size and age taken at approximately the same time after admission. CONCLUSIONS: These results indicate that early after burn injury there is a correspondence of IL-1 beta and TNF alpha with certain host responses, but these correlations disappear with the progression of illness. In general, IL-1 beta and TNF alpha appear to be poor indicators of prognosis during burn injury; however, the association of mortality with low circulating IL-1 beta values supports the concept of IL-1 beta as being an essential mediator of host defenses.     

冠状动脉综合征患者血清白细胞介素6和肿瘤坏死因子α水平及辛伐他汀的干预作用

目的:探讨辛伐他汀对急性冠状动脉综合征(acutecoronarysyndrome,ACS)患者血清白细胞介素6(IL-6)及肿瘤坏死因子α(TNF-α)水平变化的影响,以期发现上述因子变化与ACS发病的关系及辛伐他汀对ACS发病的影响。方法:2002-09/2003-09白求恩国际和平医院急诊科留观病人和河北医大第三医院心内科住院患者中符合纳入标准ACS患者52例,将ACS患者52例随机分为辛伐他汀组(n=26)和常规治疗组(n=26),分别于治疗前及治疗后3周行血清IL-6及TNF-α检测,均采用放射免疫分析方法。另选本院同期健康体检的30例作为对照组,对照组采血前2周内未服任何药物,体检时对其血清IL-6及TNF-α进行检测。结果:ACS患者治疗前血清IL-6,TNF-α水平均明显高于对照组(P<0.01)。辛伐他汀组患者治疗后血清IL-6,TNF-α水平犤(0.708±0.087)μg/L,67.73±10.00)fmol/L(犦均明显低于治疗前犤(0.800±0.083)μg/L,(79.92±14.53)fmol/L犦(P<0.01),但仍高于对照组(P<0.01)。常规治疗组患者治疗后血清IL-6,TNF-α降低不明显(P>0.05)。结论:IL-6,TNF-α水平越高,则ACS发病的概率可能越大;辛伐他汀可降低ACS患者血IL-6,TNF-α水平,具有减轻病变部位炎症反应和保护内皮的作用。     

腰椎间盘突出症患者血清白细胞介素1β及白细胞介素6和肿瘤坏死因子α变化与渗湿通络法治疗的影响：随机对照

目的：观察腰椎间盘突出症患者血清细胞因子应用渗湿通络法治疗后的变化。 方法：①对象：选择200502／12中国中医科学院望京医院收治的寒湿痹阻型腰椎间盘突出症患者43例，随机分成试验组22例和对照组21例，患者对治疗知情同意。另选择志愿参加试验的健康成年人30人为正常组。②干预：试验组患者给予渗湿通络法则下的薏苡仁汤加减（薏苡仁、杜仲、川断、木防己、威灵仙、鸡血藤、独活、牛膝、白芍等）口服，1剂／d，早晚分服，连服4周。对照组患者给予腰痛宁胶囊口服，4粒，次，1次／d，连服4周。③评估：于治疗前和4周治疗后分别应用放免法测定患者血清白细胞介素113、白细胞介素6、肿瘤坏死因子n水平；采用目测类比评分法测定患者疼痛；根据日本整形外科学会（JOA）腰痛疾患疗效评定标准判定临床疗效。 结果：①43例患者血清白细胞介素113、白细胞介素6、肿瘤坏死因子n较健康人有异常升高（P〈0．01）；治疗后试验组患者血清白细胞介素113、肿瘤坏死因子Q含量下降（P〈0．05、P〈0．01），对照组患者血清肿瘤坏死因子Q含量下降（P〈0．05）。②试验组、对照组治疗前后症状体征积分、疼痛评分均有明显改善（P〈0．01），试验组治疗前后症状体征积分、疼痛评分差值均优于对照组（P〈0．05）。 结论：应用渗湿通络法治疗后患者血清中异常升高的白细胞介素1β、白细胞介素6、肿瘤坏死因子α水平降低，疼痛症状改善明显。     

腰椎间盘突出症患者血清白细胞介素1β及白细胞介素6和肿瘤坏死因子α变化与渗湿通络法治疗的影响:随机对照

目的:观察腰椎间盘突出症患者血清细胞因子应用渗湿通络法治疗后的变化.方法:①对象:选择2005-02/12中国中医科学院望京医院收治的寒湿痹阻型腰椎间盘突出症患者43例,随机分成试验组22例和对照组21例,患者对治疗知情同意.另选择志愿参加试验的健康成年人30人为正常组.②干预:试验组患者给予渗湿通络法则下的薏苡仁汤加减(薏苡仁、杜仲、川断、木防己、威灵仙、鸡血藤、独活、牛膝、白芍等)口服,1剂/d,早晚分服,连服4周.对照组患者给予腰痛宁胶囊口服,4粒/次,1次/d,连服4周.③评估:于治疗前和4周治疗后分别应用放免法测定患者血清白细胞介素1β、白细胞介素6、肿瘤坏死因子α水平;采用目测类比评分法测定患者疼痛;根据日本整形外科学会(JOA)腰痛疾患疗效评定标准判定临床疗效.结果:①43例患者血清白细胞介素1β、白细胞介素6、肿瘤坏死因子α较健康人有异常升高(P ＜ 0.01);治疗后试验组患者血清白细胞介素1β、肿瘤坏死因子α含量下降(P ＜ 0.05、P ＜ 0.01),对照组患者血清肿瘤坏死因子α含量下降(P ＜ 0.05).②试验组、对照组治疗前后症状体征积分、疼痛评分均有明显改善(P ＜ 0.01),试验组治疗前后症状体征积分、疼痛评分差值均优于对照组(P ＜ 0.05).结论:应用渗湿通络法治疗后患者血清中异常升高的白细胞介素1β、白细胞介素6、肿瘤坏死因子α水平降低,疼痛症状改善明显.     

强直性脊柱炎患者血清介素1β、2、6及肿瘤坏死因子-α测定的意义

目的观察强直性脊柱炎（AS）患者外周血清白介素-1β（IL-1β）、白介素-2（IL-2）、白介素-6(IL-6)、肿瘤坏死因子-α（TNF-α）、红细胞沉降率（ESR）、C反应蛋白（CRP）、免疫球蛋白（IgA、IgG、IgM）水平，并分析它们与强直性脊柱炎疾病活动指数（BASDAI）相关性。 方法测定45例AS患者及30例健康体检者的IL-1β、2、6及TNF-α，CRP、IgA、IgG、IgM、ESR水平。以Bath强直性脊柱炎疾病活动指数（BASDAI）评定AS患者疾病活动性，取BASDAI中位数将患者分为活动组及非活动组，比较AS患者与对照组，活动组与非活动组各实验指标，分析它们与BASDAI的相关性。 结果AS患者ESR、CRP、IgA、IgM、IgG、IL-1β、IL-2、IL-6及TNF-α水平与对照组之间差异有统计学意义（P<0.05）。AS患者活动组CRP、IL-2与IL-6较非活动组差异有统计学意义（P<0.05）。AS患者CRP与IL-6，IL-2与IL-6，IgA与IgG两两之间成正相关，但只有IL-2、IL-6及CRP与BASDAI之间成正相关。 结论IL-2、IL-6与CRP可作为AS疾病活动性的参考指标。     

Divergent effects of tumour necrosis factor-alpha on apoptosis of human neutrophils

Apoptosis of neutrophils is a key mechanism to control the intensity of the acute inflammatory response. Previously, the cytokine TNF-α was reported by some investigators to have pro-apoptotic and by others to have antiapoptotic effects on neutrophils. The aim of this study was to explain these contradictory results.
We found that TNF-α at low concentrations strongly decreased apoptosis of neutrophils. However, at higher concentrations, TNF-α lost its protective effects, and also reversed the anti‐apoptotic effects of IFN-γ and GM-CSF. In fact, the combination of high concentrations of TNF-α with either IFN-γ or GM-CSF caused even stronger apoptosis than that seen in the presence of TNF-α alone. This 'pro-apoptotic' effect of TNF-α was blocked by anti-CD11b and was absent in neutrophils from patients with Leukocyte Adhesion Deficiency (LAD), which lack expression of β₂ integrins, and in neutrophils from patients with Chronic Granulomatous Disease (CGD), which cannot produce toxic oxygen metabolites. Under these circumstances, we found that TNF-α retained its anti‐apoptotic effects, even at high concentrations.
In conclusion, the protective effects against apoptosis of IFN-γ, GM-CSF and TNF-α itself are overruled when the concentration of TNF-α is high enough to produce a respiratory burst. This process of reactive oxygen radical formation depends on neutrophil adhesion via the β₂ integrin CD11b/CD18 and on an intact NADPH oxidase enzyme. These dual, concentration-dependent effects of TNF-α provide an explanation for previous controversial reports and support a dominant role for TNF-α in neutrophil apoptosis.     

无抽搐电休克对精神分裂症患者血清白介素6的影响

AIM: To explore the influence of modified electroconvulsive therapy on seruminterleukin-6 in schizophrenic patients. METHOD: Testing changed serumIL-6 in 60 cases treated with MECT and 60 control cases treated with clozapinetherapy by ELISA method. RESULTS: Serum H-6 level before treatment ofboth groups was positive related to SAPS; serum IL-6level wasn' trelated toBPRS total score, factor score and SANS total fractions. IL-6 level of clozapinetherapy group decrease apparently after treatment, and IL-6 level was appar-ently positive related to anxious depressed factor of BPR S; but there was noapparent difference in IL-6 level of MECT group between before and aftertreatment. CONCLUSION: To schizophrenic patients, closapine can take ef-fects of immune inhibit through inhibiting serum H-6; MECT emay have differentmechanism.