肝炎患者血清IL—2、IFN—γ和IL—10检测的意义

目的：探讨检测IL－2、IFN－γ和IL－10对病毒性肝炎患者的临床意义。方法：利用ELISA法检测97例病毒性肝炎患者血清IL－12、IFN－γ和IL－10水平，动态观察45例接受免疫增强剂治疗的慢性肝炎患者上述细胞因子的变化，结果：急性肝炎患者血清IL－12及IFN－γ水平平均明显升高（P＜0．01）；慢性肝炎、肝硬化患者血清中IL－10明显高于正常对照组（P＜0．01）。免疫增强剂治疗获得完全应答反应的患者治疗期间血清IL－12、IFN－γ水平明显上升（P＜0．01），IL－10水平下降（P＜0．05）。无应答者治疗过程中上述细胞因子无明显变化。结论：Th1型免疫应答对机体清除病毒起关键作用。Th2型免疫应答与感染慢性化及疾病持续发展有关，免疫治疗可使部分Th2型免疫应答占优势的慢性肝炎患者转化为Th1型占优势。     

病毒性肝炎患者血清IL-6,IL-8水平及临床意义

了解病毒性肝炎患者血清IL－6、IL－8水平及临床意义。应用放射免疫法检测124例病毒性肝炎患者血清IL－6、IL－8水平并动态观察，其中35例慢性肝炎进行肝活检，并按肝组织病理进行分级和分期。①急性肝炎、慢性肝炎中重度、慢性重型肝炎IL－6和IL－8水平依次升高，明显高于正常对照（P＜0．01）；②IL－6、IL－8水平与肝 组织炎症坏死程度和肝纤维化程度呈正相关（P＜0．01，P＜0．01）；③IL－6、IL－8水平随急性肝炎恢复和慢性肝炎稳定而降低（P＜0．01，P＜0．05）。IL－6、IL－8水平可作为反映肝细胞坏死程度和纤维化轻重的指标。     

病毒性肝炎患者IL-8、IL-10水平与肝功能损伤的关系

采用双抗体夹心ELISA法对76例病毒性肝炎患者的ＩＬ－８、ＩＬ－１０进行了测定。结果：各组肝炎患者ＩＬ－８检测水平显著高于正常对照组（Ｐ＜０．０５）,以ＣＨ－Ⅱ－Ⅲ组ＩＬ－８水平最高;ＣＨ－Ⅱ－Ⅲ、LC、SH三组ＩＬ－１０水平显著高于正常对照组和ＣＨ－Ⅰ组,在这三组中又以ＣＨ－Ⅱ－Ⅲ＜ＬＣ＜ＳＨ的顺序递增（Ｐ＜０．０５）。ＩＬ－８与肝炎患者的SB和ALT水平负相关。检测血清ＩＬ－８在判断病毒性肝炎患者肝脏损伤程度上有一定价值,在重型肝炎和肝炎后肝硬化联合检测ＩＬ－８、ＩＬ－１０可以预测其预后。     

慢性肺心病患者血清白细胞介素-8改变的意义

目的为探讨白细胞介素（Interleukin，IL）－8在慢性肺心病中的意义及与病情的关系。方法用ELISA方法动态观察了30例慢性肺心病患者血清IL-8水平。结果慢性肺心病患者急性加重期血清IL－8水平明显高于缓解期及正常对照（P均＜0．01），而患者在缓解期血清IL－8水平仍高于正常对照（P＜0．01）；心功能Ⅲ－Ⅳ级患者血清IL－8含量又明显高于心功能Ⅱ级患者（P＜0．01），且在急性加重期，患者血清IL－8含量与动脉血气中PaO_2和pH值均成明显的负相关性，（r分别为-0．429和-0．613，P分别＜0．02和0．01），而与PaCO_2成正相关性（r=0．889，P＜0．01）。结论IL－8可能参与了慢性肺心病的发病过程，测定血清IL－8水平，对估测慢性肺心病患者的病情轻重有一定意义。     

慢性乙型肝炎患者血清IL—40、IL—42、IL—48和IFN—γ的检测及其临床意义

目的 探讨慢性乙型肝炎病理过程中细胞因子IL-l0、IL—12、IL—18和IFN-γ血清水平的变化及其临床意义。方法 27例慢性乙型肝炎患者和25例健康人均于清晨空腹采血以双抗夹心EHSA法检测IL—10、IL—12、IL—18和IFN-γ水平并同时检测肝功能和乙肝病毒血清学指标。结果 慢性乙型肝炎患者血清IL—10、IL-l2、IL-l8和IFN-γ水平均显著高于对照组(P〈0．01)，其中慢性乙型肝炎重度患者IL—12、IL-l8和IFN-γ水平较轻中度患者显著增高(P值分别〈0．01，〈0．01，＜0．05)；HBeAg阴性组IL-l2和IL—18较HBeAg阳性组明显升高(P值分别＜0．05和＜0．01)，而IL—10和IFN-γ则无明显变化；上述各因子均与血清ALT、T—Bil呈显著正相关(r分别=0．588、0．477，0．520、0．612，0．545、0．855，0．606、0．864)，IL—12还与HBVDNA量呈显著负相关(r＝—0．51)。结论 慢性乙型肝炎患者存在异常的细胞免疫应答，IL—10、IL-l2、IL—18和IFN-γ均参与了慢性乙型肝炎的病理生理过程，并且与肝炎的病情变化密切相关。     

重型肝炎患者血清内毒素与细胞因子及细胞免疫相关性研究

检测重型肝炎患者血清内毒素（LPS）、肿瘤坏死因子-α（TNF—α）、白细胞介素-6（IL-6）、白细胞介素-10（IL-10）、白细胞介素-12（IL-12）、白细胞介素-18（IL-18）、T细胞亚群（CD4^＋、CD8^＋）。结果发现重型肝炎患者血清LPS水平明显高于健康对照组（P〈0．05），两组TNF-α、IL-6、IL-10、IL-12、IL-18水平也均有统计学差异（P〈0．05），重型肝炎患者治疗前与治疗后加重者血清LPS水平有显著差异，而TNR-α、IL-6、IL-12、IL-18水平均高于好转后，IL-10水平却在好转后升高。血浆置换后病情好转者血清LPS、IL-12、IL-18水平明显下降，TNF-α水平变化不大，病情加重者各项指标均无明显变化。表明重型肝炎患者血清LPS水平与CD4^＋／CD8^＋值呈负相关。联合检测对了解病情、判断顶后、改进治疗箫略有指导意义。     

肾综合征出血热急性期外周血细胞因子的检测及其临床意义

目的 探讨肾综合征出血热（HFRS）患者急性期外周血肿瘤坏死因子－α（TNF－α），白细胞介素－2（IL－2），白细胞介素－6（IL－6），白细胞介素－8（IL－8）含量的变化及其临床意义。方法 应用酶联方法（ELISA）对34例肾综合征出血热患者急性期外周血细胞因子进行检测。结果 HFRS患者血清TNF－α，IL－6及IL－8水平均明显高于对照组，且含量随病情加重而升高，重型组明显高于中轻型组；患者的IL－2则低于对照组，重型组较中轻型组明显降低。结论 患者血中上升的TNF－α，IL－6及IL－8和下降的IL－2水平均与该病的病理损伤有关，且与病情轻重成正相关。     

肿瘤坏死因子、白细胞介素8、可溶性细胞间粘附分子1和CD11b/CD18在良恶性胸腔积液的价值

目的 研究结核性及恶性胸腔积液患者及血清中肿瘤坏死因子（TNF）、白细胞介素－8（IL－8）、胸液中可溶性细胞间粘附分子1（sICAM-1）及外周血多形核白细胞（PMN）上粘附分子CD11d/CD18在参与胸膜病变的病理生理过程中的作用和在鉴别诊断上的价值。方法 采用放射免疫分析法（RIA法）、双抗体夹心ELISA法及流式细胞仪技术,检测31结核性、31例恶性胸腔积液患者胸液和（或）血清中TNF、IL－8、sICAM－1和CD11d/CD18表达水平,并与31例健康献血者对照。结果 结核性和恶性胸腔积液患者血清中TNF、IL－8含量以及PMN上CD11d/CD18表达显著高于正常对照组（P＜0．01）, 结核性胸液中TNF与IL－8水平和血PMN上CD11d/CD18表达明显高于恶性胸液患者（P＜0．01）,结核性胸粹中sICAM－1水平明显低于恶性胸液（P＜0．01）。胸腔积液中TNF与IL－8、sICAM－1水平呈显著正相关（r＝0．74和r＝0．79,P＜0．01）,血清TNF与PMN上CD11d/CD18的表达呈显著正相关（r＝0．61,P＜0．01）,胸腔积液中sICAM－1水平与血PMN上CD11d/CD18的表达呈显著负相关（经作曲线拟合,Y=1442．31－36．85X∧2＋0．25X∧2,R∧2＝0．59,F＝19．83,P＜0．01）。结论 细胞因子TNF、IL－8和粘附子sICAM－1、CD11b/CD18相互联系,在结核和肿瘤性胸膜病变的免疫 理生理过程中起着重要作用。它们在结核性和肿瘤性胸腔积液患者的表达水平不同,可作为临床上鉴别诊断的参考指标。     

系统性红斑狼疮患者血清IL—4和INF—γ水平的测定及其临床意义

目的：通过检测系统红斑狼疮（SLE）患者血清白细胞介素－4（IL－4）、γ－干扰素（INF－γ）的水平，探讨T淋巴细胞亚群与SLE发病的关系。方法：采用酶联免疫吸附法测定SLE患者和健康志愿者血清IL－4和INF－γ水平。结果：（1）SLE活动组血清IL－4水平和IL－4／INF－γ比值明显升高，与非活动组和对照组比较，差异有非常显著性（P＜0．001）；（2）血清INF－γ水平三组（SLE活动组、非活动组和对照组）比较，差异无显著性（P＞0．05）；（3）SLE患者激素治疗后血清IL－4水平明显降低。结论：SLE患者血清IL－4水平和IL－4／INF－γ比值明显升高，且与病情活动性相关，INF－γ水平无明显变化，活动性SLE患者存在Th2细胞优势活化状态，破坏了体内Th1/Th2正常平衡。     

病毒性肝炎患者IL-8、IL-l0水平与肝功能损伤的关系

采用双抗体夹心ELISA法对76例病毒性肝炎患者的IL-8、IL-10进行了测定.结果:各组肝炎患者IL-8检测水平显著高于正常对照组(P＜0.05),以CH-Ⅱ-Ⅲ组IL-8水平最高;CH-Ⅱ-Ⅲ、IE、SH三组IL-10水平显著高于正常对照组和CH-Ⅰ组,在这三组中又以CH-Ⅱ-Ⅲ＜LC＜SH的顺序递增(P＜0.05).IL-8与肝炎患者的SB和ALT水平负相关.检测血清IIL-8在判断病毒性肝炎患者肝脏损伤程度上有一定价值,在重型肝炎和肝炎后肝硬化联合检测IL-8、IL-l0可以预测其预后.     

Hyper-interleukin (IL)-6-naemia in haemophagocytic lymphohistiocytosis

Clinical features in patients with haemophagocytic lymphohistiocytosis (HLH) have been demonstrated to be characterized by hypercytokinaemia. Previously, we reported the impact of high serum levels of interferon (IFN)-gamma and soluble IL-2 receptor (sIL-2R) on patient outcome; however, it was not known if serum levels of interleukin (IL)-6 also could be a prognostic factor. In a study during the active phase of disease in 25 cases of HLH in children and young adults (median age 3 years, range 0.1–23 years), we noted 12 cases which showed serum IL-6 >100 (normal <4.0) pg/ml. Five of these cases showed hyper-IL-6-naemia alone without hyper-IFN-gamma-naemia (group A) whereas seven cases showed both hyper-IL-6- and IFN-gamma-naemia (group B). Patient outcome did not differ between the patients with IL-6 >100 pg/ml and those with IL-6 <100 pg/ml, suggesting that high serum concentrations of IL-6 alone do not necessarily indicate poor prognosis in patients with HLH. Among the cases with hyper-IL-6-naemia (>100 pg/ml), underlying disorders causing haemophagocytosis were found to be different between groups A and B.     

Interleukin (IL)-17 promotes macrophages to produce IL-8, IL-6 and tumour necrosis factor-alpha in aplastic anaemia

Aplastic anaemia (AA) is thought to be an autoimmune-mediated disease with active destruction of haematopoietic cells through a T helper type 1 (Th1) cell response. Interleukin (IL)-17 is a potent proinflammatory cytokine produced by activated memory T cells. Recent studies indicate that IL-17 might be an essential effector cytokine in the T-cell mediated autoimmune process. It can drive the production of tumour necrosis factor-α (TNF-α), IL-1 β, IL-6 and IL-8 by a variety of cells. The present study investigated the genetic and protein expression of IL-17 in patients with AA. The effect of IL-17 on IL-6 and IL-8 production by macrophages was also studied. AA patients showed an elevated expression of IL17A mRNA in bone marrow mononuclear cells and peripheral blood mononuclear cells. Higher IL-17 in bone marrow and peripheral blood plasma was also observed in AA patients compared with normal controls. IL-17 induced the production of IL-6 and IL-8 by macrophages both from patients with AA and normal controls. IL-17 stimulation also resulted in the production of TNF-α. These results suggested that elevated expression of IL-17 and IL-17-induced IL-6, IL-8 and TNF-α may be involved in the mechanisms of AA.     

Ethanol and murine interleukin (IL)-12 production

BACKGROUND: Interleukin (IL)-12 is a cytokine with protean effects against bacterial and intracellular pathogens. Induction of IL-12 at the time of infection has salient effects on elimination of various microbes. This work describes the effect of exposure to ethanol on lipopolysaccharide (LPS)-induced production of IL-12 in mice and whether ethanol-induced increases in IL-10 mediates these changes in IL-12 production. METHODS: BALB/c mice were pretreated with ethanol and then challenged with LPS either intravenously (iv) or intratracheally (it), and blood and lung production of IL-12 (p70 and p40 components) and serum IL-10 were assayed. Splenic and lung mRNA for IL-12 p35 and p40 components was determined. RESULTS: Ethanol pretreatment suppressed LPS-induced IL-12 p70 and p40 protein production in blood and lung. In spleen and lung, p40 mRNA was induced to a greater extent than p35 mRNA, and there was greater suppression of p40 mRNA compared with p35 mRNA in ethanol-treated animals. Ethanol up-regulated the production of IL-10, and pretreatment of these animals with a polyclonal anti-IL-10 antibody resulted in significant increases in IL-12 p70 and p40 levels, but not completely to those of control animals. CONCLUSIONS: Ethanol suppresses the production of murine IL-12 in response to LPS in blood and lung, with both the p70 and the p40 components affected. This suppression is accompanied by reductions of p40 mRNA in both spleen and lung. IL-10 may play a role in ethanol-induced suppression of IL-12, as neutralization of IL-10 partially attenuated the suppression of IL-12.     

Investigation of the interleukin (IL)-4/IL-4 receptor system in promyelocytic leukaemia PLB-985 cells during differentiation toward neutrophil-like phenotype: mechanism involved in IL-4-induced SOCS3 protein expression

The interleukin 4 (IL-4)/IL-4 receptor (IL-4R) system in promyelocytes is not well documented. Here, we used promyelocytic leukaemia PLB-985 cells differentiated with dimethylsulfoxide (PLB-985D) toward neutrophil-like phenotype to investigate the IL-4/IL-4R system. PLB-985 cells did not express CD132 (γc) but expressed the complete IL-4 type II receptor (IL-4Rα and IL-13Rα1). Moreover, PLB-985 cells lost surface expression of IL-13Rα1 during differentiation, resulting in PLB-985D cells expressing only IL-4Rα fully responsive to IL-4, as judged by activation of mitogen-activated protein (MAP) kinases and Janus kinase 1. IL-4 also increased suppressor of cytokine signalling 3 (SOCS3) protein level in the presence of the proteasome inhibitor MG132 exclusively in PLB-985D cells. As the IL-4Rα chain has been associated with a component of the phagocyte NADPH oxidase, we used PLB-985-gp91 ^phox deficient cells (mimicking chronic granulomatous disease, X-CGD), to investigate the IL-4/IL-4R system in X-CGD-D cells. IL-4 was found to activate MAP kinases in X-CGD-D cells but did not up-regulate SOCS3, in contrast to granulocyte colony-stimulating factor, granulocyte-macrophage colony-stimulating factor and IL-6. Utilization of catalase, cycloheximide and genistein inhibitors showed that IL-4 induced SOCS3 by a mechanism dependent on a complete NADPH oxidase complex, protein synthesis and tyrosine phosphorylation, but independent of production of reactive oxygen species. We conclude that IL-4 induces cell signalling in promyelocytes expressing only IL-4Rα.     

IL-10基因多态性与乙肝肝硬化易感性的相关性研究

探讨白细胞介素10(IL-10)基因多态性与乙型肝炎肝硬化易感性的关系.采用聚合酶链反应-限制性片段长度多态性(PCR-PFLP)分析方法,检测100例乙肝肝硬化患者及124例健康对照组IL-10基因启动子-1082G/A、-592A/C位点的基因多态性,并确定了其基因型和等位基因频率的分布.肝硬化组与对照组IL-10基因启动子-592A/C位点基因型分布频率和等位基因频率差异无显著性(P＞0.1),肝硬化组-1082G/A位点AA基因型频率及A等位基因频率高于对照组(P＜0.05),G等位基因相对于A等位基因患肝硬化的机会比为0.373(95%CI:0.166～0.838).IL-10基因多态性与肝硬化易感性相关,基因启动子-1082G/A位点AA基因型携带者肝硬化易感性高.     

T cells increase with gastric mucosal interleukin (IL)-7, IL-1, and Helicobacter pylori urease specific immunoglobulin levels via CCR2 upregulation in Helicobacter pylori gastritis

Background and Aims: The purpose of this study was to investigate possible factors that could impact on γδ T cell accumulation in the gastric mucosa. Method: Subjects were 22 Helicobacter pylori (H. pylori)‐free and 75 H. pylori‐infected mucosa biopsies classified into grades I～III gastritis as per our previous study. The number of γδ‐ and 45 RO‐positive T cells were determined by immunostaining. Gastric mucosal anti‐H. pylori urease specific antibodies and interleukin (IL)‐1β, IL‐2, 4, 7, 10 and IL‐12 levels were assayed by enzyme‐linked immunosorbent assay (ELISA). CC chemokine receptor 2 (CCR2) expression levels, migration, and cytokine production in γδ T cells stimulated by H. pylori urease were also evaluated. Results: The γδ T cell count was significantly higher in grade III gastritis which exhibits strong immunoglobulin (Ig)A and IgG responses to H. pylori urease with lymphoid follicles than in other groups. γδ T cell count was significantly correlated with IL‐1β and interleukin‐7 (IL‐7) levels in the gastric mucosa. H. pylori urease immunoreactivity was detected in lamina propria of grade III gastritis, along with many γδ T cells. After H. pylori eradication therapy, the γδ T cell count in grade III gastritis significantly decreased. H. pylori urease stimulated significant increases in CCR2 expression levels, although to a lesser degree than those induced by IL‐7 stimulation in both peripheral and mucosal γδ T cells. Interferon (IFN)‐γ and IL‐10 production was also stimulated by H. pylori urease in peripheral γδ T cells. Conclusions: Gastric mucosal increases in IL‐7 and IL‐1β closely corresponded to the accumulation of γδ T cells in gastric mucosa. An association was also seen between γδ T cell accumulation and H. pylori urease‐specific Ig levels.     

乙型肝炎肝硬化患者血清内毒素、IL-4、IL-18水平的研究

研究肝硬化患者病程中血清内毒素(LPS)和IL-4、IL-18水平变化。采用鲎三肽基质染色法和ELISA法分别检测35例肝硬化患者活动期和缓解期上述三项指标，并设健康人40例为对照组。结果为：肝硬化患者两期LPS、IL-4、IL-18水平均明显高于正常对照组(未检出LPS)，缓解期较活动期显著降低。三指标均呈正相关。结论：LPS、IL-4、IL-18在HBV所致肝硬化发病中可能有重要作用。