Correlation of interleukin-2 receptor and neopterin secretion in rheumatoid arthritis

Summary In rheumatoid arthritis (RA) an immuno dysregulation alters the release of neopterin from human monocytes/macrophages, probably by activation of a feed-back regulation mechanism in pterin metabolism. With the overactivation of T-lymphocytes, the secretion of interleukin-2 and its receptor (IL-2R) is influenced. Investigation on 84 RA patients has shown that this immunoactivation is accompanied by an increased secretion of neopterin and soluble IL-2R in the serum, and that both parameters are very suitable for detection of inflammatory disease activity. The significant correlation between neopterin and IL-2R (r=0.65; p0.001) in RA points out a possible connection in pathomechanisms of the immune system.     

Effects of interleukin-1, tumor necrosis factor-β, and forskolin on tissue plasminogen activator activity in human osteoblastic osteosarcoma cells

Summary The effects of interleukin-1 (IL-1), forskolin, and tumor necrosis factor (TNF-) on tissue plasminogen activator (t-PA) activity were studied in the human osteoblastic osteosarcoma cell line, G292. t-PA activity was measured in the cell media using the chromogenic substrate, S-2251. After a 24 hour incubation period, IL-1 increased t-PA in a dose-dependent manner. The effect of IL-1 at 10.0 U/ml was partially inhibited in the presence of indomethacin. Forskolin (1.0 M) increased t-PA activity after 24 hours with the effects of combined treatment of IL-1 (1.0 U/ml, 10.0 U/ml) and forskolin being apparently additive in nature. TNF- (10^-8–10^-7 M) also produced increased t-PA activity in the cell medial after a 24 hour incubation period. These results suggest that the cytokines, IL-1 and TNF-, can increase t-PA activity in G292 cells and that there is both a cAMP-dependent as well as a cAMP-independent pathway involved in the regulation of this osteoblastic cell function.     

Duodenal and jejunal atresia with agenesis of the dorsal mesentery: "apple peel" small bowel.

Two newborn infants with duodenal and jejunal atresia and agenesis of the dorsal mesentery represent our surgical experience with "apple peel" small bowel or "christmas tree" demormity. The first patient had the typical appearance of this condition. The postoperative course was complicated by hyperbilirubinemia, septicemia, and disseminated intravascular coagulation. The infant is in satisfactory condition 1.5 years after operation. The second patient had agenesis of the dorsal mesentery without spiraling of the bowel around its vascular stalk. The child died after 1 month, with complete absence of extrahepatic bile ducts as seen at a second laparotomy. Neither child had been subjected to gastrostomy.     

新生儿缺氧缺血性脑病血浆Th2 源细胞因子水平的研究

目的　研究新生儿缺氧缺血性脑病 (HIE)患儿辅助性T淋巴细胞亚群 2 (Th2 )细胞功能变化及其与HIE间的关系。　方法　采用ELISA法和单克隆抗体间接免疫荧光法 ,检测 4 6例HIE患儿不同病期血浆和外周血单个核细胞 (PBMC)体外分别产生白细胞介素 (IL) 6、IL 8、IL 10水平和T细胞IL 2受体 (IL 2R)表达率 ,并与正常足月新生儿脐血 (2 0例 )进行对照。　结果　HIE病程第 1天血浆及PBMC体外产生IL 6 [分别为 6 6 .3、80 4 .5ng L(中位数 ,以下同 ) ]、IL 8(4 10 .5、1983.6ng L)和IL 10 (2 7.9、14 0 .1ng L) ,明显高于正常脐血对照组 (分别为 1.9、187.7;91.0、76 6 .8;2 .6、16 .4ng L) (Z =4 .6 5 3～ 5 .85 6 ,P <0 .0 1) ;中重度组及并发多器官功能损害 (MOD)的HIE患儿血浆及PBMC体外产生IL 6 (分别为 86 .0、12 36 .4 ;111.3、174 6 .9ng L)、IL 8(分别为5 79.5、2 812 .2 ;5 32 .8、2 94 3.3ng L) ,分别高于轻度组 (分别为 5 2 .6、5 83.4 ;335 .3、15 2 8.9ng L)及无MOD组 (分别为 5 6 .6、713.8;35 2 .4、15 72 .4ng L)患儿 (Z =2 .2 2 8～ 2 .70 1,P <0 .0 5 ;Z =2 .877～4 .187,P <0 .0 1) ,而IL 10差异无显著性 (Z =0 .4 5 0～ 1.85 0 ,P >0 .0 5 ) ;T细胞IL 2R表达率 [(5 2 .8± 13.4 ) % ]明显     

TNF-α和IL-6对绒毛膜11β-羟基类固醇脱氢酶I型和前列腺素合成酶II型的调节

目的 :研究肿瘤坏死因子 (TNF α)、白细胞介素 6(IL 6)对胎膜糖皮质激素代谢酶 11β 羟基类固醇脱氢酶I型 (11β HSD1)和前列腺素合成酶II型 (PGHS 2 )的影响 ,以探讨细胞因子导致分娩启动的机制。方法 :利用薄层层析法 (TLC)和Westernblot杂交法分别从酶活性、蛋白表达水平 ,研究IL 6、TNF α对原代培养的人类绒毛膜细胞 11β HSD1及PGHS 2水平的影响。结果 :TNF α和IL 6对绒毛膜滋养层细胞 11β HSD1还原酶活性有促进作用 ,对绒毛膜细胞 11β HSD1和PGHS 2的蛋白表达均有上调作用。 结论 :IL 6、TNF α对胎膜 11β HSD1及PGHS 2的诱导作用可能是其导致分娩启动的机制之一     

针刺对实验性变态反应性神经炎TNF-α和IL-4的影响

目的 探讨肿瘤坏死因子-α(TNF-α)和白细胞介素-4(IL-4)与实验性变态反应性神经炎(EAN)发病的关系，从细胞因子水平研究针刺疗法对本病的免疫调节作用。方法 40只大鼠分为正常对照组、模型组、针刺组、药物组，建立大鼠EAN动物模型，观察大鼠发病率及致病程度，针刺组取腰。夹脊、足三里、悬钟穴，药物组用泼尼松灌胃给药。采用双抗体夹心ELISA法，检测大鼠血清的TNF-αa和IL-4的含量变化。结果 模型组TNF-α含量较正常组明显升高。针刺组和药物组均能降低TNF-α的含量，使其水平接近正常，尤以药物组抑制作用明显。IL-4的含量各组间均无明显差异。结论 提示本病存在Th1／Th2细胞因子间的失衡，其中以Th1型细胞占优势。针刺主要是通过抑制TNF-α等Th1细胞，来重建细胞因子间的平衡。     

The effect of interleukin-6 on enhancing the invasiveness of head and neck cancer cells in vitro

Patients with head and neck cancers that produce a high concentration of granulocyte colony-stimulating factor (G-CSF) or patients with esophageal squamous cell carcinomas who have elevated serum interleukin-6 (IL-6) concentrations have been found previously to be at significant risk for tumor invasion to adjacent organs as well as frequent metastases. This suggests that G-CSF and Il-6 enhance the invasiveness and metastatic potential of cancer cells. We studied the in vitro invasiveness of head and neck cancer cell lines with and without recombinant human G-CSF (rhG-CSF) and human IL-6 (hIL-6) in an extracellular matrix membrane system. The degree of invasiveness was affected by incubating cells with hIL-6, but not by pre-incubating the cell-matrix with hIL-6. The maximum concentration of hIL-6 for enhanced invasiveness was approximately 5,000 u/ml. In addition, rhG-CSF enhanced the invasiveness of tumor cells that produced large amounts of G-CSF. The present study also suggests that tumor cells tend to invade and metastasize in an environment rich in hIL-6. Received: 3 November 1997 / Accepted: 1 April 1998     

细胞因子基因联合放射治疗小鼠头颈部鳞状细胞癌的实验研究

目的观察白细胞介素-2(interleukin-2,IL-2)基因与白细胞介素-12(interleukin-12,IL-12)基因联合放射治疗小鼠头颈鳞状细胞癌(鳞癌)的疗效.方法模拟临床头颈肿瘤治疗方案,利用鳞癌SCCⅦ细胞株在C3H/HeJ小鼠口底建立头颈鳞癌的荷瘤动物模型,在荷瘤部位直接注射多价阳离子脂质体包裹的表达IL-2基因和IL-12基因的真核表达质粒,对照组分别注射无目的基因的空载体和磷酸盐缓冲液(phosphatic buffered saline,PBS).次日给予2 Gy直线加速器的局部肿瘤放射治疗(简称放疗).4 d后重复IL-2基因和IL-12基因局部治疗.观察肿瘤治疗前后大小变化,检测肿瘤组织中CD4+、CD8+的表达、IL-2和 IL-12的表达水平及自然杀伤(natural killer,NK)细胞和细胞毒T淋巴细胞(cytotoxic T-lymphocyte,CTL)的活性.结果 IL-2基因和IL-12基因联合加放疗治疗组肿瘤生长明显受抑制,疗效显著优于单基因加放疗治疗组、单基因治疗组和各对照组.在注射有IL-2基因及IL-12基因的治疗组中,IL-2与IL-12表达水平明显升高,小鼠脾细胞NK细胞活性和CTL杀伤活性增强,肿瘤组织内可见大片坏死,并含有大量的CD4+,CD8+淋巴细胞浸润.结论多价阳离子脂质体携带的IL-2基因和IL-12基因治疗可提高肿瘤局部和机体全身的抗肿瘤免疫应答,能加强放疗的抗肿瘤效果.