子宫内膜异位症患者瘦素检测及临床意义

目的检测子宫内膜异位症(EMS)患者血清和腹腔液瘦素(Leptin)水平的变化及在子宫内膜表达情况,探讨其在内异症发病中的作用。方法放射免疫法测定40例内异症患者和40例非内异症患者妇女(对照组1)血清和腹腔液Leptin的水平。抗生物素蛋白-过氧化物酶(SP)法检测瘦素在子宫内膜表达情况,并与R-AFS分期进行相关分析。同期检测50例健康妇女(对照组2)血清Leptin水平。结果 EMS患者血清瘦素水平与对照组间比较无差异;腹腔液中瘦素水平明显高于对照组;EMS患者和对照组子宫内膜中均有瘦素表达,EMS患者与对照组表达上存在差异(P<0.05)。结论内异症患者腹腔液中瘦素水平明显升高,并随疾病的严重程度而改变,同期影响瘦素在子宫内膜中的表达,这可能是瘦素在内异症的发生发展中起作用的机制。     

子宫内膜异位症患者腹腔液白介素13浓度与异位内膜种植关系的研究

目的　探讨腹腔液白细胞介素 - 13与子宫内膜异位症发病机制的相关性。方法　收集近一年子宫内膜异位症和良性卵巢肿瘤患者腹腔液 ,采用双抗体夹心酶联免疫吸附法 (ELISA)测定IL - 13浓度。结果　内膜异位症腹腔液中IL- 13的浓度明显低于对照组腹腔液中浓度。两组间比较P <0 .0 1,具有显著性差异。结论　内膜异位症腹腔液中IL - 13的浓度降低 ,对巨噬细胞抑制作用降低 ,可能与内异症免疫发病机制有关。     

轻症子宫内膜异位症不孕患者血清、腹腔液IL—6、EMAb的检测分析

子宫内膜异位症 (ｅｎｄｏｍｅｔｒｉｏｓｉｓ ,ＥＭ ) ,是育龄妇女的常见病、多发病 ,由ＥＭ引起不孕的发病率高达30 %～ 4 0 %。尤其目前对轻症ＥＭ不孕患者 ,是用外科还是内科治疗来提高生育力尚缺乏统一的认识 ,这其中部分原因是 :我们缺乏对ＥＭ不孕的病理生理机制的认识。为此本文探讨了轻症ＥＭ所致不孕患者的血清、腹腔液ｌＬ 6及ＥＭＡｂ水平 ,将有益于指导ＥＭ不孕的临床治疗。本文以行诊断性腹腔镜检查的 4 2例不孕患者为研究对象 ,根据术后诊断分为三组 :ＥＭ(Ⅰ /Ⅱ期 )组 16例 ;盆腔炎症组 14例 ;正常盆腔对照组 12例。采用Ｅ…     

子宫内膜异位症导致不孕的免疫因学研究

随着免疫基础研究的飞速发展，对子宫内膜异位症导致不孕的免疫病因学认识亦日渐丰富，主要表现在：子宫内膜异位症患者免疫细胞数量及功能的异常、自身抗体的产生、多种细胞因子及粘附分子含量和活性的改变、排卵机制的免疫异常等方面。     

子宫内膜异位症导致不孕的免疫病因学研究

随着免疫基础研究的飞速发展,对子宫内膜异位症导致不孕的免疫病因学认识亦日渐丰富,主要表现在子宫内膜异位症患者免疫细胞数量及功能的异常、自身抗体的产生、多种细胞因子及粘附分子含量和活性的改变、排卵机制的免疫异常等方面.     

子宫内膜异位症患者外周血和腹腔液细胞因子水平的检测及临床意义

子宫内膜异位症（简称内异症）是子宫内膜组织出现在子宫腔面以外身体的其它部位,在育龄期妇女发生率为10％-15％,其病因复杂,难以根治,容易复发,且发生率有上升趋势,因此对于内异症的发病原因越来越得到医学界的重视。近年来,许多研究表明内异症的形成和发展与免疫因素有密切关系。本文通过行腹腔镜手术并联合用药治疗的36例内异症患者术前腹腔液及术前术后外周血中的IL-6、IL-8、TNF-α水平的检测,进一步探讨其与内异症的关系,现报道如下。     

子宫内膜异位症相关性不孕的诊断及治疗研究

子宫内膜异位症是影响育龄期妇女生育能力的常见因素,其导致不孕的原因包括:腹腔液性质改变、盆腔结构异常重构、子宫内膜容受性改变等。外科手术是目前最主要的治疗手段,但子宫内膜异位症的类型、病程、程度对手术方式的选择均有影响。近年来辅助生殖技术在子宫内膜异位症相关不孕患者的治疗中,占据了越来越重要的地位。     

子宫内膜异位症不孕患者采用不同方案IVF—ET的结局分析

目的：分析采用不同方案对子宫内膜异位症不孕患者进行体外受精-胚胎移植（Invitrofertilization-embryotransfer,IVF_ET）助孕治疗结局的影响。方法：回顾性分析77例（80个周期）子宫内膜异位症患者经口服避孕药＋短方案（A组）和长方案（B组）治疗,对IVF-ET妊娠结局的影响。结果：与长方案组相比口服避孕药＋短方案组获卵数、受精率、卵裂率无显著变化（P〉0．05）,但促性腺激素（Gonadotropin,Gn）用量显著减少,临床妊娠率、胚胎植入率显著提高（P〈0．05）。结论：子宫内膜异位症患者采用口服避孕药＋短方案进行超促排卵可以提高IVF-ET的成功率。     

IL-12p70、p40在子宫内膜异位症患者腹腔液中的表达及意义

目的　通过测定子宫内膜异位症患者腹腔液中IL - 12 p70及IL - 12p4 0的水平 ,探讨其与子宫内膜异位症发生发展的关系。方法　采用酶联免疫吸附法 (ELISA)测定 2 0例子宫内膜异位症患者 (内异症组 )及 2 0例卵巢良性肿瘤患者(对照组 )腹腔液中IL - 12p70、IL - 12 p4 0的水平。比较两组间两个细胞因子水平以探讨它们与内异症发生的关系 ,并探讨其是否与疾病的进展有关。结果　腹腔液中IL - 12 p70水平内异症组稍低于对照组 ,但两者之间差异无显著性 (P >0 0 5 ) ;IL- 12 p4 0水平内异症组明显高于对照组 ,差异有显著性 (P <0 0 5 ) ;内异症组中 (Ⅰ～Ⅱ期 )患者IL - 12 p4 0水平较 (Ⅲ～Ⅳ期 )患者稍高 ,但两者差异并无显著性 (P >0 0 5 ) ;而 (Ⅰ～Ⅱ期 )患者IL - 12 p70水平明显高于 (Ⅲ～Ⅳ期 )患者 ,差异有显著性 (P <0 0 5 )。结论　内异症患者腹腔液中IL - 12p4 0水平的增高可能是自然杀伤 (NK)细胞功能受损的部分原因 ,从而可能与子宫内膜异位症的发生有一定关系 ;腹腔液中IL - 12 p70水平随内异症疾病程度进展而下降 ,表明其可能是内异症中NK细胞功能进一步下降的原因之一 ,从而可能是促使内异症进一步发展的原因之一。     

子宫内膜异位症患者腹腔液对子宫内膜细胞MHC—I类分？…

目的 分析了宫内膜异位症（ＥＭ）虱腹腔液对ＩＦＮ－γ诱导异位子宫内膜细胞上ＭＨＣ－Ｉ类抗原表达以及对正常人γδＴ细胞和自然杀伤细胞（ＮＫ）功能的影响。方法 采用免疫荧光细胞检测及细胞毒活性检测８法。结果 ＥＭ患者腹腔液对ＩＦＮ－γ诱导异位子宫内膜细胞上ＭＨＣ－Ｉ类抗原表达具有下调作用,疾病组的腹腔液对正常人外周血γδＴ细胞及ＮＫ细胞的杀伤功能具有负相调节作用。结论 子宫内膜异位症患者腹腔液中存在γ     

Immunoregulatory properties of IL-13 in patients with inflammatory bowel disease; comparison with IL-4 and IL-10

Activated monocytes with increased expression of proinflammatory cytokines play a major role in inflammatory bowel disease (IBD). Immunoregulatory cytokines such as IL-4 and IL-10 can effectively suppress the proinflammatory response of activated monocytes. IL-13 is a recently described antiinflammatory agent in vitro. The aim of our study was to determine the in vitro immunosuppressive capacity of IL-13, IL-4 and IL-10 in patients with IBD. Peripheral blood monocytes were isolated from 27 patients with ulcerative colitis (UC), 27 patients with Crohn's disease (CD) and 16 healthy controls. Cells were stimulated with pokeweed mitogen (PWM) after treatment with IL-13, IL-4 and IL-10, and secretion of IL-1β, tumour necrosis factor-alpha (TNF-α) and IL-6 was assessed using sandwich ELISA systems. Peripheral blood monocytes secreted significantly increased amounts of TNF-α and IL-6 under stimulation with PWM in patients with CD, while UC patients showed significantly elevated levels of IL-1β. The antiinflammatory cytokines IL-13, IL-4 and IL-10 were all capable of inhibiting monocyte secretion of IL-1β in a dose-dependent manner. With regard to IL-13 and IL-4, there was no significant suppression of TNF-α and IL-6 in patients with active IBD. By contrast, IL-10 was able to down-regulate all proinflammatory cytokines in active IBD as well as in controls. Proinflammatory cytokines from patients with inactive IBD could be significantly down-regulated by all three immunoregulatory cytokines. The inhibitory effect of IL-13 on TNF-α and IL-6 production in differentiated macrophages was diminished in IBD patients, as well as in controls. In disease controls we also observed a reduced inhibition of TNF-α and IL-6 after treatment with IL-13. In conclusion, the antiinflammatory activity of IL-13 is partially reduced in patients with active IBD. The hyporesponsiveness of activated and differentiated monocytes to IL-13 and IL-4 does not seem to be a disease-specific phenomenon.     

IL-13对成纤维细胞IL-13受体和IL-4受体表达的影响

目的研究IL-13对人肺成纤维细胞株HFL-1和人肝星状细胞株LX-2 IL-13受体和IL-4受体表达的调节作用。方法 RT-PCR法检测HFL-1细胞株和LX-2细胞株IL-13Rα1、IL-4R和IL-13Rα2 mRNA的表达;凝胶电泳定量软件Image Tool2.0对RT-PCR电泳条带进行光密度分析;ELISA法检测HFL-1细胞株和LX-2细胞株分泌可溶型IL-13Rα2以及检测细胞裂解液总IL-13Rα1、IL-4R和IL-13Rα2含量。结果 IL-13(5～100 ng/ml)对HFL-1细胞株和LX-2细胞株表达IL-13Rα1和IL-4R无影响;IL-13为5、10、20 ng/ml时能诱导HFL-1细胞株表达IL-13Rα2并呈现剂量依赖,当IL-13为50 ng/ml时,对HFL-1细胞株IL-13Rα2表达的诱导作用明显减弱,IL-13 100 ng/ml组没有检测到HFL-1细胞株IL-13Rα2的表达;LX-2细胞株IL-13Rα2表达缺失且IL-13不能诱导LX-2细胞株表达IL-13Rα2。结论 IL-13不能上调人肺成纤维细胞株HFL-1和人肝星状细胞株LX-2表达功能型受体IL-13Rα1和IL-4R,表明IL-13不能通过上调IL-13Rα1和IL-4R表达量来放大自身作用;一定浓度的IL-13能诱导人肺成纤维细胞株HFL-1表达抑制型受体IL-13Rα2,表明IL-13的自身负调控。     

肾病综合征患者血清IL-4和IL-10水平的变化及意义

目的通过观察肾病综合征(NS)免疫治疗前后白细胞介素-4(interleukin-4,IL-4)和IL-10水平的变化,探讨其临床意义。方法以ELISA检测52例NS患者在接受强的松和环磷酰胺治疗前及4周后血清IL-4和IL-10水平。结果NS患者血清IL-4水平显著增高(P<0.01),并与血清β_2微球蛋白呈显著正相关(n=52,r=0.352.P<0.05),血清IL-10水平与健康人无显著差异。治疗4周后血清IL-4和IL-10水平显著降低(P<0.05),尿蛋白排出量显著低于治疗前(P<0.05)。结论IL-4、IL-10参与了NS发病过程,强的松和环磷酰胺可通过调节IL-4和IL-10产生而调节NS的免疫紊乱,NS的免疫治疗方案可根据细胞因子水平(包括抗炎细胞因子IL-4和IL-10)调整。     

乙型肝炎患者血清IL-13和PGE1含量的检测及其意义

目的：通过检测乙型肝炎患者和正常对照组血清中IL-13和PGE1的水平及其与ALT、AST的相关性，探讨Ⅰ型超敏反应与乙型肝炎免疫学发病机制的关系。方法：应用酶联免疫吸附实验-双抗体夹心法，检测50例急、慢性乙型肝炎及35例正常对照组血清IL-13和PGE1水平，并观察与血清中ALT及AST水平的相关性。结果：①10例急性乙型肝炎患者血清中IL-13和PGE1含量明显高于对照组；②35例慢性乙型肝炎患者血清中IL-13和PGE1含量明显高于对照组，其中慢性重度组升高最明显，其次为中度组和轻度组；③IL-13和PGE1水平与血清ALT、AST含量均呈显著的正相关关系。结论：乙型肝炎患者血清中IL-13和PGE1水平的高低，可反映肝组织的损害程度，对病情和预后的判定也有一定的参考价值。     

支气管哮喘患者血清IL-10、IL-5和ECP的变化及其意义

目的 通过对支气管哮喘患者和正常对照组的血清IL-10, IL-5和 ECP水平的测定以及相互关系的研究,探讨它们在支气管发病中的作用.方法 应用Pharmacia UniCAP系统和ELISA方法分别测定支气管哮喘患者和正常对照组的血清E CP和IL-10、IL-5水平.结果 正常对照组和发作期的支气管哮喘患者的 ECP水平分别为(3.97±2.13) μg/L和(21.76±12.08) μg/L.正常对照组,支气管哮喘ECP 升高组和支气管哮喘ECP正常组的血清IL-5水平分别为(10.90±4.41) pg/mL,(20.62± 15.7 4) pg/mL和(9.24±7.16) pg/mL.正常对照组和支气管哮喘ECP升高组之间IL-5水平有显著差异(P＜0.01),正常对照组和支气管哮喘ECP正常组之间IL-5水平无差异(P＞0.05) ,支气管哮喘ECP正常组和ECP升高组之间IL-5水平有显著差异(P＜0.01),ECP与IL-5 明显相关 ,两者之间的相关系数r=0.465(P＜0.01).正常对照组,支气管哮喘ECP升高组和支气管哮喘ECP正常组的血清IL-10水平分别为(38.28±15.17) pg/mL,(22.76±15.25) pg/mL 和(42.32±14.61) pg/mL,支气管哮喘ECP正常组和ECP升高组之间IL-10水平有显著差异( P＜0. 01).结论 支气管哮喘的发生与嗜酸粒细胞有密切的关系,ECP和IL-5可反映嗜酸粒细胞的活化程度,在支气管哮喘发作时嗜酸粒细胞处于激活状态,易于释放蛋白颗粒;IL-5对嗜酸粒细胞有调控作用.支气管哮喘组的血清IL-10水平较正常对照组低,提示支气管哮喘患者IL-10分泌减少,不能有效抑制炎症或促炎症细胞因子的合成及释放,亦即不能有效抑制炎症反应,可能是导致或加重气道炎症的原因之一.     

IL-13和IL-4在哮喘发病中的作用及相互关系

目的　探讨IL 13在哮喘发病中的作用及其与IL 4的相互关系。方法　哮喘组 2 4例 ,男 17例 ,女 7例 ;健康对照组 2 4例 ,男 12例 ,女 12例。用ELISA法检测不同时段PBMC培养上清IL 13和IL 4水平及加IL 13单克隆抗体 (McAb)和IL 4McAb干预后PBMC培养上清IL 4、IL 12、IL 13和IFN γ水平。结果　 (1)IL 13动态变化 :①对照组PBMC培养 3d、5d、7d水平均较培养 1d水平高 ,差异有显著性 ,培养 3d的水平较培养 5d、7d的高 ,差异有显著性 ;②哮喘组PBMC培养 3d、5d、7d的水平均较培养 1d的水平高 ,差异有显著性 ,培养 5d的水平均较培养 3d、7d的水平高 ,但之间差异无显著性 ;③哮喘组PBMC培养 3d、5d、7d的IL 13水平均较对照组高 ,差异有显著性。 (2 )IL 4动态变化 :①对照组和哮喘组PBMC培养 1d后 ,IL 4水平明显上升 ,第 3天仍保持较高水平 ,第 5、7天明显下降 ;②哮喘组 1d、3d、5d和 7d水平均较对照组高 ,差异有显著性。 (3)IL 4McAb干预后 ,哮喘组和正常组IL 13水平与对应小鼠IgG组相比有显著性降低 ,哮喘组IFN γ水平与对应小鼠IgG组相比有显著性增高。 (4)IL 13McAb干预后IL 12水平在哮喘组和正常组均提高 ,与对应小鼠IgG组相比差异有显著性。 (5 )IL 13McAb和IL 4McAb联合干预后哮喘组I     

IL-4, IL-10 and IL-13 down-regulate monocyte-chemoattracting protein-1 (MCP-1) production in activated intestinal epithelial cells

Several studies have demonstrated that intestinal epithelial cells play a major role in the initiation and perpetuation of intestinal inflammation by secreting proinflammatory cytokines and chemokines. MCP-1 is suggested to be a chemokine that plays a major part during intestinal inflammation in inflammatory bowel disease (IBD). Immunoregulatory cytokines such as IL-4, IL-10 and IL-13 have been described to exert anti-inflammatory properties on various cell types. The aim of our study was to determine the effect of Th2 cytokines on the production of MCP-1 by activated intestinal epithelial cells. We examined Caco-2 cells as well as intestinal epithelial cells which were isolated from surgical specimens. Production of the chemokine MCP-1 was determined under stimulated and non-stimulated conditions. IL-4, IL-10 and IL-13 were added to stimulated epithelial cells under various culture conditions. Supernatants were analysed for cytokine concentrations using ELISAs. Under stimulation with physiological agents like IL-1β or tumour necrosis factor-alpha (TNF-α), we observed markedly increased concentrations of MCP-1 in supernatants of Caco-2 cells and intestinal epithelial cells. IL-4, IL-10 and IL-13 all had the capacity to down-regulate the production of MCP-1 in Caco-2 cells as well as in freshly isolated epithelial cells. Caco-2 cells which were primed with Th2 cytokines 24 h before stimulation were subsequently decreased in their ability to be stimulated by IL-1β or TNF-α for MCP-1 production. As MCP-1 has been shown to play a major role during intestinal inflammation, the in vitro suppression of MCP-1 in enterocytes suggests the in vivo use of regulatory cytokines in patients with active IBD.     

IL-4、IL-13蛋白表达及抗IL-4、IL-13人源单链抗体的筛选

目的:表达IL-4和IL-13蛋白,从人源单链抗体文库中分别筛选抗IL-4和抗IL-13单链抗体.方法:采用RT-PCR从健康志愿者外周血单核细胞(PBMC) mRNA中扩增IL-4和IL-13 cDNA;构建硫氧还蛋白融合表达载体,转化大肠杆菌BL21,IPTG诱导表达并对表达产物进行纯化鉴定.以生物素化的IL-4和IL-13为抗原从前期构建的人源抗体文库中采用噬菌体展示技术分别筛选抗IL-4和抗IL-13人源单链抗体(scFv).结果:扩增的IL-4 cDNA大小为280 bp,表达的融合蛋白大小为27 kD左右.扩增的IL-13 cDNA大小为252 bp,表达的融合蛋白大小为25 kD左右.分别以生物素化的IL-4和IL-13蛋白为抗原,采用噬菌体展示技术对人源抗体文库进行3轮富集后,分别有大约37％的scFvs与IL-4有结合特性,有约27％的scFvs与IL-13有结合特性.筛选了4株分别与IL-4和IL-13结合能力强的单链抗体进行了Westem blot鉴定和测序.结论:成功筛选到抗IL-4和抗IL-13人源性单链抗体.     

Single Nucleotide Polymorphisms in IL-10, IL-12p40, and IL-13 Genes and Susceptibility to Glioma

Glioma is one of the most aggressive and most common tumors of the central nervous system (CNS) in humans. The exact causes of glioma are not well known, but evidence suggests the involvement of genetic factors in addition to environmental risk factors. The present study aimed to determine whether polymorphisms in IL-10-1082A/G, IL-12p40 1188C/A, and IL-13+2044G/A (rs20541) are associated with the incidence of glioma in Iraqi patients. Ninety-six patients with different grades of glioma and 40 apparently healthy individuals were recruited. A blood sample and genomic DNA were collected from all subjects. The amplification refractory mutation system and sequence-specific primer polymerase chain reaction (PCR) were used for genotyping of IL-10-1082A/G and IL-12p40 1188C/A, respectively; whereas, the IL-13+2044G/A was detected by DNA sequencing after amplification of the genes by PCR.All SNPs were within Hardy-Weinberg equilibrium and each appeared in three genotypes in patients and controls. In IL-10-1082A/G, these genotypes frequencies were AA (75%), AG (22.93%) and GG (2.07%) in patients as compared to similar frequencies (62.5%), (27.5%) and (10%) respectively, in controls. The variant IL-12p40 1188C/A genotype was AA (72.92%), AC (23.96%), and CC (3.13%%) in patients as compared to 65%, 30%, and 5%, respectively, in controls. The frequencies of IL-13+2044G/A genotypes (GG, GA, and AA) were 89.58%, 9.37%, and 1.04% among patients versus 47.5%, 32.5% and 20%, respectively, among controls. These results suggest a protective role of mutant alleles G and A in IL-10-1082A/G and IL-13+2044G/A against gliomas. Further studies with more rigorous parameter designs will be needed to confirm the current findings.     

谷氨酰胺、地塞米松对内毒素血症大鼠血清IL-8,IL-10的影响

目的通过观察谷氨酰胺、地塞米松对内毒素血症大鼠血清IL-8,IL-10的影响,探讨地塞米松、谷氨酰胺对内毒素血症大鼠的保护途径.方法选健康18日龄Wistar大鼠120只,随机取8只腹腔注射生理盐水作对照组(0h),余大鼠按腹腔注射药物不同分成内毒素(L)、谷氨酰胺预防(Gln)地塞米松治疗(D1)组,每组40只,各组于加LPS后2、4、6、24及72h分别断头取血,用放免法测定IL-8,IL-10.结果(1)L组IL-8在2、24h出现两次升高,前者升高程度更明显,差异显著,P<0.01;D1和C1n组各时间点IL-8均低于L组,尤其以2h抑制作用更强,差异显著,P<0.01;Gln组第一次高峰在6h.(2)L组IL-10在2、72h出现两次升高,后者升高程度更明显,差异显著,P<0.01;D1和Gln组第二次升高均提前至24h,增幅最高的为D1组,而其它各时间点IL-10均以Gln组升高明显,差异显著,P<0.01.结论细胞因子IL-8/IL-10在内毒素血症中起主要的损害与抗损害作用,地塞米松治疗对机体能抑制损伤/促进修复;谷氨酰胺不仅有与地塞米松相似的作用,而且可使损伤延迟,二者都能使修复作用提前.