Graves'病患者血清IFN-γ、IL-2及IL-6的动态观察

目的：通过动态观察Graves’病患者血清IFN-γ、IL-2及IL-6的含量变化，探讨细胞因子在Graves’病发病中的作用。方法：应用化学发光免疫分析测定血FT3、FT4、TSH含量，放射免疫分析测定IL-2、IL-6含量，双抗体夹心ELISA法测定IFN-γ含量，分析其与Graves’病的关系。结果：治疗前GD患者、GD复发者外周血IFN-γ、IL-6均高于正常对照组（P〈0．01），IL-2低于对照组（P〈0．01）；缓解组外周血IL-6明显下降，IL-2明显升高，均接近正常对照组，IFN-γ含量虽然有所下降，但仍然明显高于对照组（P〈0．01）。GD治疗前外周血IFN-γ、IL-6含量与FT3、FT4呈直线正相关，IL-2含量与FT3、FT4呈直线负相关。结论：细胞因子是认识Graves’病发病机理的重要线素，细胞因子与Graves’病的病程及病情控制密切相关，细胞因子对于估价Graves’病的病情、协助诊断及判断愈后有一定的指导意义。     

孕酮对自然流产小鼠白细胞介素6表达的影响

目的:探讨孕酮对自然流产小鼠母胎界面白细胞介素6(IL-6)的调节作用.方法:建立经典的自然流产动物模型(CBA/J×DBA/2),用免疫组织化学显色和RT-PCR检测自然流产小鼠蜕膜及绒毛组织中IL-6蛋白和mRNA的表达情况.结果:孕酮组血清孕酮水平明显高于模型组,IL-6水平高于模型组.孕酮组血清孕酮、IL-6水平与正常组比较均无差异.免疫组织化学显色和RT-PCR结果显示,在绒毛组织中,孕酮组IL-6蛋白相对含量显著高于模型组,IL-6 mRNA相对含量高于模型组,两者与正常组比较均无差异;在蜕膜组织中,孕酮组IL-6蛋白的相对含量低于模型组,IL-6 mRNA相对含量高于模型组,与正常组比较均无差异.结论:孕酮通过上调IL-6的表达来减少自然流产的发生和发展,而且孕酮调节Th1/Th2细胞因子平衡的作用发生在母胎界面.     

TPA致小鼠耳肿胀模型的中性粒细胞聚集及IL-1β、IL-6、TNF-α、IL-17A的表达水平研究

目的从蛋白水平和mRNA水平探讨佛波酯(TPA)诱导的小鼠炎症耳组织中IL-1β、IL-6、TNF-α和IL-17A的表达情况。方法通过HE染色观察TPA致小鼠耳组织的炎症水肿和淋巴细胞浸润,测定髓过氧化物酶(myeloperoxidase,MPO)活性判断中性粒细胞的聚集情况,ELISA法检测IL-1β、IL-6、TNF-α、IL-17A的蛋白含量以及实时荧光定量PCR法检测它们的mRNA水平。结果与正常组相比,模型组小鼠耳组织有明显的炎症水肿和淋巴细胞浸润,中性粒细胞聚集严重,并且该组小鼠耳组织中IL-1β、IL-6、TNF-α的含量和mRNA水平显著地增高,而IL-17A没有明显地变化;阳性药物组与模型组相比,能有效地抑制小鼠耳组织的炎症水肿,淋巴细胞浸润,中性粒细胞聚集以及下调各炎症细胞因子的蛋白含量和mRNA水平。结论 TPA诱导的小鼠耳肿胀严重程度除了与淋巴细胞浸润和中性粒细胞聚集有关外,还与靶组织中显著上调的IL-1β、TNF-α和IL-6蛋白含量和mRNA水平有关。     

GBEE对荷瘤小鼠IL-2、IL-12、TNF-α及TGF-α水平的影响

目的:研究银杏外种皮提取物(GBEE)的抗肿瘤作用及其对荷瘤小鼠免疫功能的影响。方法:采用ICR小鼠,建立S180移植瘤模型,GBEE连续灌胃16天,观察荷瘤小鼠移植瘤抑制率;体外培养荷瘤小鼠脾脏细胞,应用LPS诱生IL-12,应用ConA诱生IL-2;采用双抗体夹心ABC-ELISA法测定IL-12及荷瘤小鼠血清TNF-α含量;采用MTT法检测IL-2活性;采用放射免疫分析法测定荷瘤小鼠血清TGF-α的含量。结果:GBEE可明显抑制小鼠S180移植瘤的生长,其中200 mg/(kg.d)剂量组抑瘤率达38.36%;GBEE可提高荷瘤小鼠血清TNF-α含量,促进脾淋巴细胞IL-12的形成,增强脾脏T淋巴细胞IL-2活性,降低荷瘤小鼠血清TGF-α水平。结论:GBEE可抑制瘤细胞分泌TGF-α,具有显著抗肿瘤作用;可促进细胞因子IL-2、IL-12和TNF-α的生成,具有增强荷瘤机体免疫功能的作用。GBEE的免疫增强效应可能是其发挥抗肿瘤作用的重要途径之一。     

IL-23/IL-17炎症轴在咪喹莫特诱导的小鼠银屑病样皮肤损害中的作用

 目的：观察IL-23/IL-17炎症轴在咪喹莫特诱导的小鼠银屑病样皮损形成过程中的作用及变化规律。方法：雌性BALB/c小鼠随机分为正常对照组和咪喹莫特组,采用PASI评分观察银屑病样小鼠模型皮损动态变化;光镜观察皮损组织形态学变化;细胞因子抗体芯片技术对比检测两组小鼠血清及皮损组织中细胞因子谱的变化;采用流式细胞小球微阵列术、实时荧光定量PCR和蛋白免疫印迹分析技术对小鼠血清及皮肤组织中细胞因子含量、mRNA和蛋白表达水平进行检测;流式细胞术分析外周血及脾细胞成分。结果：咪喹莫特诱导小鼠产生红斑、鳞屑、增厚等典型的银屑病样皮损,并随着给药时间的延长呈现一个抛物线型的动态变化;经咪喹莫特外用刺激后,小鼠皮肤及血清中IL-23/IL-17轴相关细胞因子、Th1、Th2和Treg类细胞因子含量及表达水平均显著升高。IL-23/IL-17轴细胞因子表达也呈现一个先升高后降低的动态变化过程。咪喹莫特组小鼠外周血及脾细胞中树突状细胞比例显著升高,脾细胞中Th17细胞比例升高,约为正常对照组的3～4倍,Treg细胞比例约为正常对照组的2倍。结论：咪喹莫特诱导小鼠产生的皮损症状、病理学特征及细胞因子改变都与银屑病相似,是进行银屑病研究可行的动物模型,该模型制备后第1～8天可模拟疾病的发展阶段。Th17细胞活化及IL-23/IL-17轴参与了该模型皮损的形成,并呈现一个先升高后降低的动态变化过程。Th1细胞介导的炎症反应也参与了该模型皮损的形成,并且伴随Treg 和Th2类细胞因子的反馈性升高。     

肝硬化患者血清IL-6、IL-10和HA、PⅢP检测的临床意义

目的：探讨了肝硬化患者血清IL-6、IL-10和HA、PⅢP水平的变化及临床意义。方法：分别应用放免法和ELISA法对61例肝硬化患者进行了血清IL-6、IL-10和HA、PⅢP含量检测并与30名正常人作比较。结果：肝硬化患者血清IL-6、IL-10和HA、PⅢP含量均非常显著地高于正常人组（P〈0．01）,相关分析昆示,肝硬化患者血清HA、PⅢP水平与IL-6、IL-10 呈明显正相关（r=0．6216、0．5127、0＋4875、0．4715,P〈0．01）。结论：细胞因子IL-6、IL—10在肝纤维化形成中发挥重要作用,在早期肝纤维化的诊断中具有一定的临床实用价值。     

Graves病小鼠模型IL-10水平与Th17细胞功能的检测和意义

目的 研究Th17细胞及相关细胞因子IL-17 mRNA与IL-10 mRNA在实验性Graves小鼠体内变化.方法 利用TSHR-E(胞外区)的腺病毒免疫小鼠方法建立Graves疾病模型,化学发光法检测血清FT4水平,细胞培养生物学方法检测TSAb活性,流式细胞术(FCM)分析小鼠脾脏细胞中Th17细胞的比例,qRT-PCR检测小鼠脾脏细胞中IL-17和IL-10mRNA水平.结果 小鼠血清FT4及TSAb水平升高,TSAb与FT4水平呈显著正相关(r=0.90,P＜0.01);Graves小鼠脾细胞中Th17细胞的比例为(2.56±0.43)％,明显高于正常对照组小鼠(1.07±0.27％)％(P＜0.05);Graves小鼠脾细胞中IL-17 mRNA的含量明显高于正常对照组(P＜0.05),而IL-10 mRNA的含量明显低于正常对照组(P＜0.05);且IL-17和IL-10水平变化存在明显的负相关(r=-0.564,P＜0.01).结论 TSHR-E(胞外区)的腺病毒免疫建立的GD模型中,IL-17mRNA增加和IL-10 mRNA则明显下降;提示两者可能在GD的发生及发展中发挥免疫调节作用.     

尖锐湿疣患者治疗前后血清IL-2、IL-6和TNF-α水平检测的临床意义

为探讨尖锐湿疣患者治疗前后的血清IL-2、IL-6、TNFα-水平及其临床意义,分别应用RIA法和ELISA法对42例尖锐湿疣患者测定血清IL-2、IL-6和TNFα-水平,并与30名健康人(正常组)作比较。结果表明,尖锐湿疣患者在治疗前血清TNF-α水平显著高于正常组(P<0.01),而IL-2、IL-6则显著低于正常组(P<0.01),经6个月治疗后,与正常组比较仍有显著性差异(P<0.05)。结论:尖锐湿疣患者的免疫功能存在明显缺陷。     

支气管哮喘患儿治疗前后外周血Th1／Th2相关细胞因子的临床分析

目的：探讨支气管哮喘患儿治疗前后外周血Th1／Th2相关细胞因子水平的变化及临床意义。方法i应用放射免疫分析和酶联法对31例支气管哮喘患儿进行了外周血中Th1型细胞因子（IL-2、IFN-1）和Th2型细胞因子IL-4、IL-10浓度,并与35名正常人组作比较。结果i支气管哮喘患儿在治疗前血清IL-2、IFN-^y水平均非常显著地低于正常儿组（P〈0．01）,而血清IL4、IL-10水平又非常显著地高于正常儿组（P〈0．01）。经治疗1个月后则与正常儿组比较无显著性差异（P〉0．05）。结论：支气管哮喘患儿存在Th1／Th2细胞免疫失衡。Th1免疫功能低下。IFN-1下调可能是参与哮喘发病机制的重要原因,对哮喘有负向调节作用。哮喘患儿存在Th2细胞免疫功能亢进,以IL-4、IL-10为代表的Th2免疫功能在儿童哮喘的发病中发挥正性促炎作用。     

慢性肾衰患者血清IL-18、IL-10、sIL-2R、TNF-α水平变化

目的：研究CRF患者血清IL-18、IL-10、TNF-α、sIL-2R的水平变化及临床意义。方法：分别采用RIA和ELISA法检测CRF患者血清IL-18、IL-10、TNF-α、sIL-2R含量，并与正常对照组比较分析。结果：CRF患者血清IL-18、IL-10、TNF-α、sIL-2R明显高于正常对照组（P〈0．01）。结论：CRF患者多种细胞因子水平升高，血清IL-18和TNF-α水平升高提示了CRF的发生发展过程，而IL-10和sIL-2R升高则对其肾脏功能有一定的保护作用。     

Cytokine-specific ELISPOT assay single cell analysis of IL-2, IL-4 and IL-6 producing cells

In order to assess cytokine-producing cells at the single cell level, the cytokine-specific ELISPOT assay has proven to be an important and sensitive method. The purpose of this study was to adapt this method to elucidate individual cells producing murine IL-2, IL-4 or IL-6. In order to establish these cytokine-specific ELISPOT assays, IL-2-, IL-4- and IL-6-specific cDNA transfected myeloma cell lines, e.g., X63-Ag8-653 X2, X63-Ag8-653 X4 and X63-Ag8-653 X6, respectively, were used as specific cytokine-producing cells. In the IL-2 ELISPOT assay, the coating reagent, monoclonal antibody (mAb) rat IgG2a anti-mouse IL-2 (CR #40014) was used while rabbit IgG polyclonal anti-mouse IL-2 was employed for detection of IL-2 spot forming cells (SFC). The mAbs anti-mouse IL-4, BVD4-1D11 and BVD6-24G2 were selected as capture and detection antibodies for enumeration of IL-4 SFC. For the IL-6 ELISPOT assay, anti-mouse IL-6 (MP5-20F3) mAb was used for coating and MP5-32C11 mAb was used for detection of IL-6 SFC. When IL-2 producing X63-Ag8-653 X2 cells were subjected to these three different ELISPOT assays, IL-2-specific SFC were only noted with the IL-2 ELISPOT system. In the case of IL-4 SFC, only X63-Ag8-653 X4 cells formed specific spots using the tandem of BVD4-1D11 and BVD6-24G2 mAbs. IL-6-specific spots developed in MP5-20F3 mAb pre-coated wells containing X63-Ag8-653 X6 cells, when developed with mAb anti-IL-6 (MP5-32C11). Addition of cycloheximide (50 μg/ml) inhibited formation of IL-2, IL-4 and IL-6 SFC by approximately 90%. When an unrelated mAb was used as detection antibody in these three different cytokine-specific ELISPOT assays, IL-2-, IL-4-and IL-6-specific SFC were not detected. Further, when concanavalin A stimulated T cells from Peyer's patch of normal mice were subjected to the respective cytokine-specific ELISPOT assay, IL-2, IL-4 and IL-6 SFC were enumerated. These results have shown that cytokine-specific IL-2, IL-4 and IL-6 ELISPOT assays have now been established and will allow analysis of the frequency of cytokine-secreting cells at the single cell level.     

卵巢癌细胞IL-6、IL-8及其受体表达的研究

目的分析比较五种常见的上皮性卵巢癌细胞系IL-6、IL-8及其受体表达的差异。方法IL-6、IL-8的表达分别采用RT-PCR和ELISA法进行检测，IL-6受体（IL-6Rα和gp130）及IL-8受体（IL-8RA和IL-8RB）的表达采用免疫印迹技术进行测定。结果①五种上皮性卵巢癌细胞均组成性表达IL-6和IL-8。IL-6和IL-8在CAOV-3细胞中的表达水平均最高，而在HO-8910PM细胞中的表达水平均最低，IL-6在SKOV-3、HO-8910、OVCAR-3细胞中的表达水平依次降低，IL-8在OVCAR-3、SKOV-3、HO-8910细胞中的表达水平依次降低。②五种上皮性卵巢癌细胞均表达IL-6Rα、gp130及IL-8RA；除CAOV-3细胞外，其它细胞均表达IL-8RB。结论本研究旨在筛选表达IL-6和IL-8及其相应受体的细胞株，为研究IL-6、IL-8与卵巢癌发生、发展关系奠定基础，同时也为今后卵巢癌的免疫治疗提供一个新的思路。     

脑胶质瘤的MRI影像表现及其与IL-17、IL-24、VEGF、GFAP的相关性研究

目的探讨脑胶质瘤的MRI影像表现及其与脑胶质瘤组织中白细胞介素-17(IL-17)、白细胞介素-24(IL-24)、血管内皮生长因子(VEGF)、胶质纤维酸性蛋白(GFAP)阳性表达的相关性。方法回顾性分析我院神经外科68例经手术病理证实为脑胶质瘤患者的临床资料并将其纳入研究组,以79例因脑出血行开颅手术患者为对照组。分析研究组患者的MRI影像表现并通过HE染色、免疫组化SP法检测2组患者中IL-17、IL-24、VEGF、GFAP表达的差异性,应用Speraman等级相关分析IL-17、IL-24、VEGF、GFAP表达与MRI表现的关系。结果脑胶质瘤位于大脑半球者65例(95.59%),脑胶质瘤位于小脑半球者3例(4.41%)。66例(97.06%)表现为T1WI低、T2WI混杂信号伴周围中—重度水肿,2例(2.94%)表现为T1WI稍高、T2WI混杂信号;肿瘤内出血31例(45.58%),无出血37例(54.42%);2例(2.94%)表现为轻度水肿,2例(2.94%)表现为中度水肿,64例(94.12%)表现为重度水肿;44例(64.71%)脑胶质瘤内见流空血管影,脑胶质瘤生长速度快,瘤体均较大,最大截面为0.7 cm×1.2 cm~10.3 cm×9.6 cm,形态不规则。DWI呈弥散受限改变66例(97.06%),无弥散受限2例(2.94%);增强扫描后均匀强化59例(86.76%),不均匀9例(13.24%);59例(86.76%)呈花环状或花瓣状明显强化,环壁部分呈栅栏状,9例(13.24%)呈轻度结节状强化。IL-17、VEGF在对照组中不表达,研究组IL-17、VEGF表达阳性率高于对照组,IL-24、GFAP表达阳性率低于对照组,差异均有统计学意义(P<0.05)。Speraman等级相关分析显示,IL-24、GFAP表达阳性率随脑胶质瘤分级升高呈下降趋势,呈显著负相关(r=-0.711、-0.577,P<0.05);IL-17、VEGF表达阳性率随脑胶质瘤分级升高呈上升趋势,以Ⅳ型胶质瘤表达最高,呈显著正相关(r=0.670、0.614,P<0.05)。结论脑胶质瘤MRI表现具有瘤体大、累及脑叶多、形态不规则,信号不均匀,水肿明显的特点,肿瘤组织中IL-17、IL-24、VEGF、GFAP的阳性表达能够反映脑胶质瘤分级程度。     

Increased IL-2, IL-4 and interferon-gamma (IFN-gamma) in steroid-sensitive nephrotic syndrome.

We investigated the production of cytokines by peripheral blood mononuclear cells (PBMC) and serum cytokine concentrations in children with steroid-sensitive idiopathic nephrotic syndrome (SSNS). PBMC from patients off treatment were collected during remission and relapse and cultured in medium alone or stimulated with calcium ionophore plus phorbol myristate acetate. Control PBMC were taken from healthy age-matched children. IL-2 was measured by bioassay, IL-4 by immunoradiometric assay, and IL-8 and IFN-gamma by ELISA. After 24 h culture without stimulation, IL-2, IL-4 and IFN-gamma were not detectable in the supernatant in any of the children. After stimulation, the supernatant concentrations of IL-2 (median 172 U/ml at 24 h) and IL-4 (160 pg/ml at 24 h; 210 pg/ml at 72 h) were significantly increased in relapse compared with remission (IL-2 37 U/ml; IL-4 65 pg/ml and 60 pg/ml) and controls (IL-2 69 U/ml; IL-4 40 pg/ml and 40 pg/ml) (P < 0.05). The concentration of IFN-gamma was not significantly increased in relapse compared with remission and controls (600, 325, and 145 U/ml, respectively, at 72 h). IL-8 concentrations were similar in relapse, remission and controls with stimulation (median 32, 40 and 40 ng/ml, respectively) and without (30, 17 and 10 ng/ml). IL-2 was not detectable in serum, but IL-4, IL-8 and IFN-gamma were measurable in about half the patients, both in relapse and remission, though were virtually undetectable in controls. We conclude that relapse of SSNS in children is associated with T lymphocyte activation with release of IL-2, IL-4 and IFN-gamma.     

Leptin, IL-10 and inflammatory markers (TNF-alpha, IL-6 and IL-8) in pre-eclamptic, normotensive pregnant and healthy non-pregnant women

PROBLEM: Despite progress in immunobiology, pre-eclampsia (PE) remains one of the most common reasons for women to die during pregnancy. The widespread pathophysiological mechanisms are endothelial dysfunction, oxidative stress and inflammation. The aim of this study was to assess the alteration in the levels of leptin, interleukin (IL)-10 and inflammatory cytokines [tumour necrosis factor (TNF)-alpha, IL-6 & IL-8] in pre-eclamptic (severe and mild), healthy pregnant and non-pregnant women and correlate these parameters with disease severity. METHOD OF STUDY: The levels of leptin, IL-10 and inflammatory cytokines were measured by high sensitivity enzyme-linked immunoabsorbant assay. The study subjects were 54 pre-eclamptic women (ten severe and 45 milder), compared by age matched 50 healthy pregnant and 27 non-pregnant women. Kruskal-Wallis non-parametric analyses of variance followed by Mann-Whitney U-test were used for statistical analysis. RESULTS: The levels of leptin, TNF-alpha, IL-6 & IL-8 in pre-eclamptic subjects were increased significantly when compared with the healthy control pregnant and non-pregnant (P < 0.000). The concentration of IL-10 has shown different pattern as its level decreased significantly (0.001) in pre-eclamptic women (overall) in comparison with control subjects (pregnant & non-pregnant). A combination of 80% or higher sensitivity and specificity was seen in the parameters analysed, except IL-8 and IL-10. CONCLUSION: Our findings suggest a relationship among TNF-alpha, IL-6, IL-8, IL-10 and leptin and indicate that altered levels of above markers in PE might be used as markers of pro-inflammation/anti-inflammation and endothelial dysfunction in pre-eclamptic pregnancies. These results also advocate the abnormal leptin and cytokine responses in mother, which might be involved in the pathogenesis of PE.     

A multidonor ELISPOT study of IL-1 beta,IL-2, IL-4, IL-6, IL-13, IFN-gamma and TNF-alpha release by cryopreserved human peripheral blood mononuclear cells

Utilization of cryopreserved peripheral blood mononuclear cells (PBMCs), rather than fresh ones collected from the same donor on different dates, overcomes the variability in sensitivity of these cells to activation agents. To understand the effect of cryopreservation, frozen PBMCs from eight healthy donors were studied to release T(H)1 or T(H)2 cytokines including IL- 1 beta, IL-2, IL-4, IL-6, IL-13, TNF-alpha and IFN-gamma using ELISPOT assay. The number of spot-forming cells (SFC) was determined using three concentrations of PBMCs (5 x 10(6), 5 x 10(5) and 5 x 10(4) cells/ml). PBMCs from all eight donors were found to retain their functional capacity to release T(H)1 or T(H)2 cytokines after freezing and thawing. When PBMCs were taken in concentrations 5 x 10(6) or 5 x 10(5) cells/ml, the density of IL-1 beta-, IL-2-, IL-6- and TNF-alpha-related spots in a well for most of the donors appeared to be overly high, making SFC quantification either difficult or impossible. To the contrary, PBMCs in concentration 5 x 10(4) produced distinct and quantifiable spots. The density of spots related to IL-4 and IL-13 release appeared to be optimal for SFC quantification when PBMCs were taken in concentration 5 x 10(6) whereas in 5 x 10(5) cells/ml the spot density was very low and absent in 5 x 10(4) cells/ml concentration group. No relationship between release levels of different cytokines was found, except IFN-gamma and IL-2 cytokine indicating that cryopreserved PBMCs with a high IFN-gamma response will likely have a high IL-2 response as well. Our results indicate that a release level of one cytokine may not be reliably predicted by knowing the level of the other. This implies that it is necessary to test cryopreserved PBMCs in a broad range of concentrations to determine one, which will be optimal for producing distinct and quantifiable spots.     

Chronic mucocutaneous candidiasis. I. Altered antigen-stimulated IL-2, IL-4, IL-6 and interferon-gamma (IFN-γ) production

Patients with chronic mucocutaneous candidiasis (CMC) present with persistent infections with the opportunistic yeast Candida. Impaired cell-mediated responses to Candida have been documented in CMC patients, but the defect remains poorly understood. The importance of Th1 cytokines in resistance and Th2 in susceptibility to Candida infections has recently been demonstrated in murine models. In our studies we evaluated production of IL-2 and IFN-γ (markers of Th1 type responses) as well as IL-4 and IL-6 (Th2 type markers) following stimulation with two kinds of Candida antigens (CAgs), polysaccharide antigens, tetanus toxoid and pokeweed mitogen. Our results demonstrate that CMC patients have impaired cytokine production upon in vitro stimulation with CAgs resulting in low or absent IL-2, increased IL-6 and either absent or increased IFN-γ production. Cytokine production following stimulation by other antigens was unaltered. The overall cytokine-producing capacity assessed through mitogen stimulation was also intact. Addition of IFN-α or IFN-γ to culture in an attempt to modify cytokine production did not have significant effects. Levels of soluble IL-6 receptors were not increased and could not account for increased IL-6 production. Our studies support the hypothesis that Candida antigens trigger a predominantly Th2 instead of a Th1 cytokine response in patients with CMC.     

脂多糖刺激下大鼠腹膜间质细胞IL-18、IL-6的表达和氧化应激的影响

目的:研究脂多糖刺激下大鼠腹膜间皮细胞(RPMC)IL-18、IL-6和氧化应激产物丙二醛(MDA)的表达。方法:原代培养RPMC,用不同浓度脂多糖(1、10、100 mg/L)刺激RPMC 6 h;10 mg/L脂多糖刺激RPMC 3、6、12、24 h。用real time-PCR法检测IL-18mRNA的表达,ELISA法检测细胞上清液中IL-18和IL-6的蛋白水平,硫代巴比妥酸法检测细胞中MDA的含量。结果:与正常对照组比较,脂多糖刺激下RPMC IL-18、IL-6和MDA的表达明显增加(P<0.05),且呈浓度依赖性;随着刺激时间的延长,上述指标呈递增趋势,IL-18于12 h达高峰。结论:脂多糖刺激下RPMC促炎症因子IL-18、炎症因子IL-6及氧化应激产物MDA的表达均增加,引起持续放大的炎症氧化反应,损伤腹膜导致超滤失败。     

急性结膜炎患者治疗前后血清hs-CRP、IL-6、IL-10、IL-18检测的临床意义

目的:探讨了急性结膜炎患者治疗前后血清hs-CRP、IL-6、IL-10、IL-18水平的变化及意义.方法:分别应用放免法、免疫比浊法和酶联法对38例急性结膜炎患者进行了血清hs-CRP、IL-6、IL-10和IL-18水平检测,并与35名正常健康人作比较.结果:急性结膜炎患者在治疗前血清hs-CRP、IL-6、IL-10和IL-18水平均非常显著地高于正常人(P＜0.01),经2周的抗炎治疗后则与正常人比较无显著性差异(P＞0.05).结论:检测急性结膜炎患者血清hs-CRP、IL-6、IL-10和IL-18水平的变化对临床观察预后有重要的临床价值.     

Regulatory effect of e2, IL-6 and IL-8 on the growth of epithelial ovarian cancer cells

To determine the regulatory effects of estrogen and cytokine IL-6 and IL-8 on the growth of epithelial ovarian cancer （OVCA）, we first examined the status of estrogen receptors （ERα and ERβ）, IL-6 receptor （IL-6Rα and gp130）, and IL-8 receptor （IL-8RA and IL-8RB） on five epithelial OVCA cell lines by semiquantitative RT-PCR and Western blot analysis. Results showed that the expressions of these receptors were variable on the five cells. Those OVCA ceUs expressing the receptors were selected to study related molecular mechanism. MTT assay was performed to observe the effects of 17β-estradiol （E2）, IL-6 and IL-8 on cell proliferation. We discovered that E2 markedly promoted the proliferation of CAOV-3 and OVCAR-3 cell in a time- and dose-dependent manner. Tamoxifen （Txf）, an ER inhibitor, completely blocked the proliferation of the E2-induced cells, and IL-6- or/and IL-8-neutralizing antibody only showed partially blocking activity. IL-6 and IL-8 were able to significantly stimulate CAOV-3 and OVCAR-3 cell proliferation in a time- and dose-dependent manner, which had a potential synergistic effect on CAOV-3 cells but not on OVCAR-3 cells. The cell proliferation induced by these two cytokines was abolished completely by their specific neutralizing antibodies, partially by Txf, but not by unrelated goat IgG. Taken together, our results suggested that estrogen, IL-6 and IL-8 could modulate OVCA growth by forming a reciprocal cascade with amplifying effect.