重症肌无力患者白细胞介素6水平的测定

目的　探讨白细胞介素 6 (IL 6 )在重症肌无力 (MG)发病机制中的作用。方法　采用双抗体夹心ELISA法对 18例MG患者用糖皮质激素 (GC)治疗前、治疗 3个月后和 2 0例正常对照血清IL 6、乙酰胆碱受体抗体 (AchRab)水平进行检测。结果　MG患者组血清IL 6水平显著高于对照组 (P <0 .0 1) ,MG患者组血清IL 6水平在用GC治疗 3个月后显著降低 (P <0 .0 1) ,其血清IL 6与血清AchRab水平呈正相关 (r =0 .6 89,P <0 .0 1)。结论　IL 6与MG发病密切相关 ,IL 6参与了MG的免疫病理过程 ;检测血清IL 6水平对MG临床有重要价值 ;GC可抑制IL 6合成及Ach Rab的产生。     

幽门螺杆菌及白细胞介素-6与初发脑梗死的关系

目的　观察幽门螺杆菌 (Hp)感染及血清白细胞介素 6 (IL 6 )的浓度与初发脑梗死的关系 ,探讨Hp感染可能导致脑梗死的机制。方法　采用病例对照 1∶1配对的研究方式 ,检测 80例初发脑梗死患者(观察组 )和对照组血清标本的Hp特异性抗体IgG(Hp IgG)、IL 6及C 反应蛋白的浓度。 结果　观察组81% (6 5 / 80 )、对照组 5 8% (46 / 80 )Hp IgG阳性 ,两者比较有显著性差异 (χ2 =10 .31,P <0 .0 1,OR =3.38,95 %CI为 1.6 1～ 7.0 9) ;观察组的Hp IgG、IL 6浓度均明显高于对照组 (均为P <0 .0 1)。Hp IgG浓度与IL 6浓度正相关 (r =0 .6 6 ,P <0 .0 1) ,与C 反应蛋白浓度正相关 (r =0 .5 8,P <0 .0 1) ,与临床神经功能缺损评分正相关 (r =0 .74 ,P <0 .0 1)。结论　Hp感染与初发脑梗死的发生有关 ,脑梗死发病后血清Hp IgG浓度亦升高 ,且随Hp IgG浓度的升高血清IL 6、C 反应蛋白浓度亦相应升高 ,患者的临床神经功能缺损程度也越重。     

白果对哮喘小鼠血清中白细胞介素5作用的研究

目的 :探讨白果对哮喘小鼠血清中白细胞介素 5 (IL - 5 )的作用。方法 :BALB/C小鼠经鸡卵蛋白免疫建立哮喘模型 ,并于激发前 1h腹腔注射 0 .1%白果注射液 0 .15ml,通过ELISA法检测血清中IL - 5的含量。结果 :致敏组小鼠血清中IL - 5水平高于正常对照组 (P <0 .0 5 ) ;治疗组小鼠血清中IL - 5水平较致敏组低 (P <0 .0 5 )。结论 :白果注射液可降低哮喘小鼠血清中IL - 5水平 ,是一种值得进一步探讨的平喘中药     

支气管哮喘患者IL-4、IL-5及血清IgE水平的变化

目的　探讨支气管哮喘患者血清白细胞介素 4 (IL 4 )、白细胞介素 5 (IL 5 )、IgE水平及不同病程的差异。方法　采用酶联免疫吸附试验 (ELISA)检测了支气管哮喘患者经植物血凝素 (PHA)刺激的外周血单介核细胞 (PBMC)培养上清液中IL 4、IL 5水平 ,同时用散射比浊法进行IgE检测。 结果　支气管哮喘患者经PHA刺激的PBMC培养上清液中IL 4、IL 5及IgE较对照组明显增高 ,差异有显著性 ;哮喘发作期IL 4、IL 5、IgE水平较缓解期明显升高 ,差异有显著性。结论　IL 4、IL 5与支气管哮喘的发生密切相关。     

白细胞介素-8及白细胞介素-10与支气管哮喘发病关系的研究

目的 探讨白细胞介素－8（IL－8）及白细胞介素－10（IL－10）在支气管哮喘发病机制中的作用。方法 搜集30例支气管哮喘急性发作期患者，28例支气管哮喘缓解期患者和20例健康者的静脉血，离心后取血清，采用放射免疫法测定其中IL－8及IL－10水平，同时对以上人员常规测定血中PO2，PCO2以及一秒钟用力呼气容积占预计值百分比（FEV1占预计值％），并把它与IL－8及IL－10进行相关性比较。结果 支气管哮喘急性发作期患者血清IL－8水平明显高于缓解期及健康对照组，IL－10水平明显低于缓解期及健康对照组，均有显著性差异。而哮喘急性发作期患者治疗后血清IL－8水平明显低于治疗前，血清IL－10明显高于治疗前。支气管哮喘急性发作期患者FEV1占预计值％明显低于其它两组，有显著性差异。血清中IL－8水平与FEV1占预计值％呈负相关，而IL-10水平与FEV1占预计值％呈正相关。结论 IL－8与IL－10参与了支气管哮喘气道炎症反应。     

支气管哮喘患者血清IL-37、IL-25、IgE的变化及意义

【目的】探讨支气管哮喘患者血清白细胞介素（IL ）‐37、IL‐25、免疫球蛋白 Ig E的表达及意义。【方法】收集支气管哮喘患者急性发作期（发作期组）、缓解期（缓解期组）及健康体检者（对照组）的静脉血标本,采用双抗体夹心ELISA法检测血清IL‐37、IL‐25、IgE的水平并比较。【结果】支气管哮喘急性发作期组血清IL‐37水平显著低于缓解期组及对照组,血清IL‐25、Ig E水平显著高于缓解期组及对照组,差异有统计学意义（ P ＜0．05）。哮喘急性发作期患者血清IL‐25水平与Ig E之间呈正相关（ r ＝0．673, P ＜0．05）,血清IL‐37水平与IgE之间呈负相关（ r ＝－0．487,P ＜0．05）。【结论】哮喘成人血清IL‐37、IL‐25、IgE水平能反应哮喘气道炎症活动情况及疾病严重程度,三者显著相关。     

老年慢性气管炎患者血清及痰液白细胞介素水平的检测及其意义

目的 :探讨老年慢性支气管炎患者血清及痰液白细胞介素水平变化及其意义。方法 :以放射免疫法测定 42例老年慢性支气管炎急性发作患者 ,3 7例老年慢性支气管炎缓解期患者以及 3 1例健康对照者血清及痰液中IL 2、IL 4、IL 6、IL 8水平 ,并对以上三组上述细胞因子水平进行统计学分析。结果 :急性组与缓解组血清与痰液中IL 4、IL 6、IL 8水平均高于正常对照组 (P <0 0 5 ) ,其中 ,急性组血清与痰液中上述细胞因子水平较对照组更高(P <0 0 5 )。但是 ,急性组与缓解组IL 2水平低于正常对照组 (P <0 0 5 ) ,其中 ,急性组较缓解组更低 (P <0 0 5 )。同时 ,直接相关分析表明 ,急性组血清IL 6与IL 8、IL 6与IL 4呈正相关关系 (P <0 0 5 ) ;痰液中IL 4、IL 6、IL 8相互间呈正相关关系 (P <0 0 5 )。结论 :IL 2、IL 4、IL 6、IL 8均参与老年慢性支气管炎的发病机制 ,在慢性气道炎症病理过程及急性发作中起着重要作用。这些指标的测定对于老年慢性支气管炎的诊断及炎症反应评估有一定的临床价值。     

心力衰竭患者血浆白细胞介素18的检测及临床意义

目的　探讨充血性心力衰竭 (CHF)患者血浆白细胞介素 18(IL - 18)水平的变化及临床意义。方法　采用ELISA法检测 4 8例CHF患者血浆IL - 18水平 ,以 30例健康者做比较 ,分析CHF患者治疗前后血浆IL - 18水平的变化及不同心功能的CHF患者血浆IL - 18水平的变化。结果　CHF患者血浆IL - 18水平显著高于正常对照组 (t =4 .4 5 0 ,P <0 .0 1) ,治疗后显效者血浆IL - 18水平显著下降 (t =9.384 ,P <0 .0 0 1) ,不同心功能的CHF患者血浆IL - 18水平差异显著 (F =2 5 0 .75 9,P <0 .0 1) ,随心功能恶化而升高 (P <0 .0 2～ 0 .0 0 1)。结论　IL - 18可能参与CHF的发生及发展过程。     

白细胞介素-4、白细胞介素-8、白细胞介素-9在支气管哮喘患儿血清中的表达及临床意义

目的 观察白细胞介素(IL)-4、IL-8、IL-9在支气管哮喘患儿血清中的表达,并探讨其临床意义.方法 选取支气管哮喘急性发作期、临床缓解期患儿各43例,分别设为发作组和缓解组,另选取同期体检健康儿童37例作为对照组,检测所有儿童的血清IL-4、IL-8、IL-9水平.结果 IL-4、IL-8、IL-9在对照组、缓解组、发作组儿童血清中的表达水平均呈递增趋势,组间比较均有显著差异(P＜0.01).结论 血清IL-4、IL-8、IL-9水平与支气管哮喘的发生、发展过程密切相关,临床可作为支气管哮喘病情进展的参考指标.     

老年支气管哮喘患者血清中白细胞介素及肿瘤坏死因子的检测及意义

目的探讨白细胞介素-4（Interleukin-4,IL-4）、白细胞介素-8（Intedeukin-8,IL-8）、白细胞介素-10（Interleukin10,IL-10）和肿瘤坏死因子-α（Tumor necrosis factor,TNF-α）水平在支气管哮喘患者发病机制中的作用。方法选择支气管哮喘急性发作期患者组26例和缓解期患者组22例,健康人（对照组）22例的血清。采用双抗体夹心ELISA法分别测定血清中IL-4、IL-8、IL-10和TNF-α水平的变化。结果支气管哮喘急性发作期和缓解期患者血清中IL-4、IL8、IL-10和TNF-α水平明显升高,与对照组比较差异有显著性（P〈0．01）,但急性发作期和缓解期患者血清中IL-8相比较无显著性差异（P〉0．05）。结论测定IL-4、IL-8、IL-10和TNF-α的水平可作为判断哮喘疾病程度的重要参考指标,为探讨支气管哮喘发病机制奠定理论基础。     

Ⅰ期尘肺患者血清白细胞介素12、白细胞介素12p70、白细胞介素10和白细胞介素18含量的变化

目的探讨血清白细胞介素12(IL-12)、白细胞介素12p70(IL-12p70)、白细胞介素10(IL-10)和白细胞介素18(IL-18)水平在Ⅰ期尘肺发生发展中的作用。方法采用双抗体夹心酶联免疫吸附测定(ELISA)法检测79例Ⅰ期尘肺患者(其中包括44例煤工尘肺患者和35例矽肺患者)、42例具有相同接尘史但未患尘肺的井下煤矿工人(接尘对照)及41例井上健康查体人员(正常对照)的血清IL-12、IL-12p70、IL-10和IL-18的含量。结果矽肺组IL-12和IL-10水平明显高于两对照组,组间差异有统计学意义(均P<0.05);煤工尘肺组IL-12和IL-10水平虽高于两对照组,但差异均无统计学意义(P>0.05);煤工尘肺组和矽肺组IL-12p70水平较两对照组均明显增高,差异具有统计学意义(P<0.01);而IL-18水平在各组间无明显改变(P>0.05)。煤工尘肺Ⅰ期、矽肺Ⅰ期及其对应的Ⅰ期合并高血压、冠心病和Ⅰ期并发慢性阻塞性肺疾病中4项指标水平比较,其差异无统计学意义(均P>0.05);煤工尘肺Ⅰ期和矽肺Ⅰ期患者不同接尘年限间比较,4项指标水平均未发现明显改变(P>0.05)。Ⅰ期尘肺患者血清IL-12、IL-12p70及IL-10三者之间呈正相关,而与IL-18均无相关性。结论Ⅰ期尘肺患者体内细胞因子网络紊乱可能与尘肺发病机制有关。     

Helicobacter pylori infection enhances mucosal interleukin-1β, interleukin-6, and the soluble receptor of interleukin-2

It is thought thatHelicobacter pylori colonization of the gastric mucosa might stimulate the production of several cytokines, which might trigger and maintain the gastric inflammation associated withHelicobacter pylori infection. In the present study we evaluated interleukin-1β, interleukin-6, and the soluble receptor of interleukin-2 both in mucosal homogenates and in the sera ofHelicobacter pylori-infected (39 cases) and uninfected (40 cases) patients to investigate whether there was any relationship between variations in cytokines and (1) the severity ofHelicobacter pylori-associated gastritis or (2) CagA-positiveHelicobacter pylori strains. Mucosal, but not serum levels of interleukins-1 and-6 and interleukin-2 receptor were significantly higher in infected than uninfected patients, Serum levels ofHelicobacter pylori antibodies were significantly higher in infected than uninfected patients, These levels correlated with mucosal interleukin-1β. The degree of antral or body inflammatory grade was higher in infected than in uninfected patients; cytokines levels were higher in patients with high-grade gastritis, most of whom wereHelicobacter pylori positive. Patients infected with CagA-positive strains also had higher levels of interleukin-1β, but not of interleukin-2 receptor or interleukin-6. In conclusion,Helicobacter pylori infection results in a local increase in interleukins-1β and-6 and interleukin-2 receptor associated with high-grade mucosal inflammation. Interleukin-1β seems to favor anti-Helicobacter pylori antibody production, and mucosal levels are enhanced mainly in patients infected with cytotoxicHelicobacter pylori strains.     

Blocking interleukin-1 receptors

Summary During inflammation, injury, immunological challenge or infection, interleukin-1 appears to mediate, in part, the pathogenesis, of disease. Most studies on interleukin-1 are derived from experiments in which bacterial products, such as endotoxins from Gram-negative bacteria or exotoxins from Gram-positive organisms, are used to stimulate macrophagic cells. In general, several cytokines are induced by microbes to their products. Although cytokines are thought to play a role in the outcome of disease, only a few have been directly implicated as mediators of the pathogenic mechanisms of the host. Studies on specific inhibition of interleukin-1 activity have employed interleukin-1 receptor antagonist, interleukin-1 receptors blocking antibodies or soluble interleukin-1 receptors. Experiments in vitro, in animal models of disease and in human subjects have shed considerable light on a critical role for interleukin-1 in the pathogenesis of disease. This review focuses on interleukin-1 as a cytokine of strategic importance to the outcome of disease, particularly inflammatory and infectious diseases.     

Interferon-gamma differentially regulates interleukin-12 and interleukin-10 production in leprosy.

The ability of monocytes to influence the nature of the T cell response to microbial pathogens is mediated in part by the release of cytokines. Of particular importance is the release of IL-12 and IL-10 by cells of the monocyte/macrophage lineage upon encountering the infectious agent. IL-12 promotes cell mediated immunity (CMI) to intracellular pathogens by augmenting T-helper type 1 responses, whereas IL-10 downregulates these responses. The ability of IFN-gamma to modulate the balance between IL-12 and IL-10 production was examined by studying leprosy as a model. In response to Mycobacterium leprae stimulation, IFN-gamma differentially regulated IL-12 and IL-10 production resulting in upregulation of IL-12 release and downregulation of IL-10 release. Furthermore, we determined that the mechanism by which IFN-gamma downregulates IL-10 was through the induction of IL-12. The data suggest a model of lymphocyte-monocyte interaction whereby the relative presence or absence of IFN-gamma in the local microenvironment is a key determinant of the type of monocyte cytokine response, and hence the degree of CMI in the host response to infection.     

烧伤患者血浆白介素-8和白介素-10水平的变化

目的：观察严重烧伤患者血浆白介素 ８（ＩＬ ８）和ＩＬ １０ 水平的变化,探讨其与烧伤后全身感染的关系。方法：收集１９ 例严重烧伤患者的血浆,利用酶联免疫吸附（ＥＬＩＳＡ）法测定血浆中ＩＬ ８ 和ＩＬ １０ 水平。结果：烧伤后患者血浆ＩＬ ８ 和ＩＬ １０ 水平急剧升高;非脓毒症患者血浆ＩＬ ８ 和ＩＬ １０ 水平在伤后逐渐降至正常,而脓毒症组患者则急剧升高。３ 例死于脓毒症者血浆ＩＬ ８ 和ＩＬ １０ 持续在高水平状态。结论：烧伤能诱导机体产生ＩＬ ８ 和ＩＬ １０;过高的ＩＬ １０ 可能与烧伤后感染有关     

Lentiviral-mediated interleukin-4 and interleukin-13 RNA interference decrease airway inflammation and hyperresponsiveness

Interleukin (IL)-4 and IL-13 are two key cytokines released from activated T helper type 2 (Th2) cells and strongly associated with asthma and allergic disease. We applied silencing of the IL-4 and IL-13 gene expression by RNA interference delivered by a lentiviral vector to evaluate the therapeutic role of IL-4 and IL13 short hairpin RNAs (shRNAs) in a murine model of asthma. Mice were sensitized with ovalbumin (OVA), and one treatment of IL-4 and IL-13 shRNA lentiviral vector (Lenti-si-IL-4 and Lenti-si-IL-13) was instilled intratracheally 48?hr before challenge. After three challenges of OVA antigen, mice were assessed for airway inflammation and hyperresponsiveness. With infection of Lenti-si-IL-4 and Lenti-si-IL-13 in EL-4 cells, both RNA and protein expressions of IL-4 and IL-13 were obviously abrogated. Furthermore, intratracheal instillation of Lenti-si-IL-4 and Lenti-si-IL-13 in OVA-immunized mice resulted in a strong inhibition of local IL-4 and IL-13 cytokine release. Treatment with Lenti-si-IL-4 and Lenti-si-IL-13 successfully alleviated OVA-induced airway eosinophilia and Th2 cell cytokine release. Finally, to determine airway hyperresponsiveness by enhanced pause and pulmonary resistance in noninvasive and invasive body plethysmography, we found that administration of Lenti-si-IL-4 and Lenti-si-IL-13 markedly decreased airway hyperresponsiveness in OVA-immunized mice. These results suggest that inhibition of IL-4 and IL-13 gene expression by shRNA lentiviral vector markedly inhibits antigen-induced airway inflammation and hyperresponsiveness in mice.