急性脑梗死患者颈动脉粥样硬化斑块与IL-6及CRP的关系

目的分析急性脑梗死患者颈动脉粥样硬化斑块性质与白细胞介素-6(IL-6)、C反应蛋白(CRP)表达水平的关系。方法选择急性脑梗死患者95例(观察组)为研究对象,根据颈动脉彩色多普勒超声检测结果分为不稳定斑块组(29例)、稳定斑块组(31例)及无斑块组(35例),选择同时期健康人30例为正常对照组,测定4组研究对象血清中IL-6、CRP的水平并进行比较。结果观察组CRP(4.80±2.16)mg/L和IL-6(209.54±75.60)pg/mL水平显著高于正常对照组的(2.43±0.51)mg/L和(103.34±8.99)pg/mL(P0.05)。不稳定斑块组CRP、IL-6水平均高于稳定斑块组、无斑块组和对照组(P0.05);稳定斑块组高于无斑块组和对照组(P0.05)。CRP、IL-6水平与动脉粥样硬化斑块的不稳定性呈正相关(rCRP=0.740,rIL-6=0.924,均P0.05)。结论急性脑梗死患者颈动脉粥样硬化斑块性质与IL-6、CRP表达水平密切相关,可能在预测脑血管病的发生及防治中起重要作用。     

白细胞介素和基质金属蛋白酶对颈动脉粥样硬化斑块易损性及脑梗死的影响

目的探讨炎细胞因子白细胞介素17、10(IL17、IL10)和基质金属蛋白酶12(MMP12)与颈动脉粥样硬化斑块易损性及脑梗死的关系。方法根据临床卒中事件将70例患者分为无症状性颈动脉粥样硬化(ACAS)组和急性动脉粥样硬化性脑梗死(AACI)组,并根据颈部血管彩色超声结果分为易损性斑块组和非易损性斑块组,酶联免疫吸附试验测定各组受试者血清IL17、IL10和MMP12水平。结果各组患者血清IL17、IL10及MMP12表达水平比较,差异均有统计学意义(P=0.000)。其中AACI组患者血清IL17及MMP12分别高于ACAS组和正常对照组(均P=0.000),而AACI组患者血清IL10表达水平低于正常对照组和ACAS组(均P=0.000),后两组之间差异无统计学意义(P=0.275)。易损性斑块组患者血清IL17和MMP12表达水平高于非易损性斑块组(P=0.000,P=0.014),而血清IL10表达水平低于非易损性斑块组和正常对照组(P=0.000),后两组之间差异无统计学意义(P=0.742)。相关分析显示,血清IL17表达水平与MMP12呈正相关(r=0.640,P=0.000)、与IL10呈负相关(r=0.430,P=0.000),MMP12与IL10之间呈负相关(r=0.242,P=0.013)。结论 IL17、IL10及MMP12均参与了动脉粥样硬化及其脑梗死的病理过程,IL17、MMP12水平升高及IL10水平下降与斑块易损性密切相关,其结果有助于临床早期发现动脉粥样硬化斑块的易损性及预测急性缺血性脑卒中事件的发生。     

急性脑梗死患者血清IL-35、MMP-9与颈动脉粥样硬化斑块稳定性的关系

目的探讨急性脑梗死患者血清白细胞介素-35(IL-35)、基质金属蛋白酶9(MMP-9)与颈动脉粥样硬化斑块稳定性的关系。方法选择急性脑梗死患者89例,应用彩色多普勒超声检查颈动脉斑块,根据颈动脉粥样硬化斑块稳定性分为易损斑块组和稳定斑块组。采用酶联免疫吸附法检测患者血清IL-35、MMP-9水平,并分析IL-35、MMP-9与斑块稳定性的关系。结果颈动脉粥样硬化易损斑块组的患者41例,稳定斑块组的患者48例。易损斑块组血清IL-35水平(17.89±7.21 ng/ml)明显高于稳定斑块组(9.08±3.45 ng/ml)(P<0.05)。MMP-9水平易损斑块组(430.36±72.78 ng/ml)亦显著高于稳定斑块组(305.16±45.63 ng/ml)(P<0.01),差异均有统计学意义。结论脑梗死患者血清IL-35、MMP-9水平可能与颈动脉斑块稳定性有关。     

急性脑梗死患者颈动脉斑块稳定性与血浆IL-18、MMP-9的相关性研究

目的 探讨急性脑梗死(ACI)患者颈动脉斑块稳定性与血清白细胞介素-18(IL-18)、基质金属蛋白酶-9(MMP-9)变化的相关性.方法 收集ACI患者200例,另选择相匹配的80名健康体检者为健康对照组.应用彩色多普勒超声检查颈动脉内膜-中膜厚度(ITM)及斑块类型,根据检查结果分为斑块组与非斑块组,其中斑块组分为不稳定斑块组和稳定斑块组两亚组.测定所有观察对象血清IL-18、MMP-9水平,分析各组间IL-18及MMP-9水平的差异,并分别对IL-18、MMP-9水平与颈动脉斑块的稳定性级别(稳定性斑块、不稳定性斑块的斑块稳定性级别分别定义为1级和2级)进行Spearman相关性分析.结果 斑块组139例(包括不稳定斑块组96例、稳定斑块组43例),非斑块组61例.不稳定斑块组患者血清IL-18、MMP-9水平[分别为(230.56±41.79)pg/mL、(90.97±30.08)μg/L]高于稳定斑块组[分别为(209.87±38.67)pg/m L、(66.81±28.67)μg/L](t=2.7595、t=4.4416,均P＜0.01);稳定斑块组IL-18、MMP-9水平高于非斑块组[分别为(171.48±22.51)pg/mL、(47.54±29.03)μg/L] (t=5.8488、t=3.3507,均P＜0.01)及对照组[分别为(167.42±26.47) pg/mL、(39.92±25.99)μg/L](t=6.4337、t=5.2766,均P＜0.01);非斑块组与对照组比较血清IL-18、MMP-9水平差异无统计学意义(t=0.9616、t=1.6394,均P＞0.05).血清IL-18水平、MMP-9水平均与颈动脉斑块稳定性级别相关(分别r=0.4531,P＜0.01;r=0.4588,P＜0.01).结论 ACI患者血清中IL-18、MMP-9水平与颈动脉斑块的稳定性相关.     

强化降脂治疗对急性脑梗死患者血清炎症因子hs-CRP、IL-8、IL-6及MMP-9水平的影响

目的 探讨短期内使用阿托伐他汀强化降脂对急性脑梗死患者血清高敏C反应蛋白(hs-CRP)、白细胞介素-8(IL-8)、白细胞介素-6(IL-6)及基质金属蛋白酶-9(MMP-9)的影响,以了解其对脑梗死炎症抑制和颈动脉斑块稳定作用.方法 120例急性脑梗死患者患者根据颈动脉超声检查结果分为颈动脉稳定斑块组(n=60)和颈动脉易损斑块组(n=60).抽血检查后随机分为常规治疗组60例(阿托伐他汀10mg/d,口服)和强化治疗组60例(阿托伐他汀40mg/d,口服).所有患者药物治疗前和治疗后2w检测血脂及血清hs-CRP、IL-8、IL-6和MMP-9水平.结果 治疗前常规治疗组和强化治疗组中血脂及血清hs-CRP、IL-8、IL-6和MMP-9水平差异无显著性(均P＞0.05).治疗后2w,强化治疗组中LDL-C、血清hs-CRP水平明显低于常规治疗组,差异具有著性(P＜0.01),强化治疗组中两亚组(尤其是易损斑块组)血清IL-8、IL-6和MMP-9水平明显低于常规治疗组,差异具有显著性(P＜0.01).结论 阿托伐他汀强化降脂能迅速降低脑梗死患者的血清炎症因子水平,具有抑制炎症和稳定斑块的作用.     

慢性精神分裂症患者血清IL-2、IL-4和IL-10水平及与精神症状的相关性

目的探讨慢性精神分裂症患者血清白细胞介素2(IL-2)、白细胞介素4(IL-4)和白细胞介素10(IL-10)的水平变化及其与精神症状的相关性。方法于2012年12月-2013年10月在广州医科大学附属脑科医院采用抽签法选取符合《国际疾病分类(第10版)》(ICD-10)诊断标准的40例慢性精神分裂症住院患者为患者组,同期通过广告招募64例健康对照者为对照组。采用酶联免疫吸附试验(ELISA)检测两组血清IL-2、IL-4和IL-10水平,采用阳性和阴性症状量表(PANSS)评估患者组的精神症状。结果患者组血清IL-2水平高于对照组[(25.85±6.06)pg/m L vs.(12.63±1.90)pg/m L],差异有统计学意义(P0.05);两组血清IL-4水平[(7.36±1.54)pg/m L vs.(8.76±3.13)pg/m L]和IL-10水平[(4.29±0.87)pg/m L vs.(3.76±1.17)pg/m L]比较,差异均无统计学意义(P均0.05);患者组血清IL-2、IL-4和IL-10水平与病程、住院时长、抗精神病药治疗剂量及PANSS评分均无线性相关(P均0.05)。结论慢性精神分裂症患者的血清IL-2水平高于健康对照者,IL-4和IL-10水平与对照者比较未见差异;IL-2、IL-4和IL-10水平与患者的精神症状未见线性相关性。     

多发性硬化患者下丘脑-垂体-肾上腺轴功能改变的临床研究

目的：观察多发性硬化（multiple sclerosis ,MS）患者下丘脑‐垂体‐肾上腺轴（hypothalamo‐pituitary‐adrenal axis ,HPAA）的功能改变情况。方法选择作者医院60例非急性发作期MS患者（MS组）,以同期作者医院门诊健康体检者30名为健康对照（对照组）,采用酶联免疫吸附法（enzyme linked immunoassay ,ELISA ）检测早晨8点空腹血皮质醇（cortisol ,CORT ）、促肾上腺皮质醇激素（adrenocorticotropin ,ACT H ）、促肾上腺皮质醇激素释放激素（corticotropin releasing hormone ,CRH）水平。MS组患者根据EDSS评分的不同,分为EDSS＞4.5组（10例）和EDSS≤4.5组（50例）两组;根据 MS分型,分为复发缓解型 MS （relapsing‐remitting multiple sclerosis ,RRMS）组（48例）和非复发缓解型MS（非RRMS）组（12例）两组。结果与对照组〔（55.67±32.48） ng/mL〕比较,MS组CORT 〔（121.09±89.46） ng/mL〕表达升高（P＝0.000）,与对照组〔（252.91±129.76） pg/mL〕比较,MS组ACTH〔（158.66±92.94） pg/mL〕表达下降（P＝0.024）。不同性别之间上述指标比较差异无统计学意义（均 P＞0.05）。EDSS评分＞4.5组〔（75.74±36.69） pg/mL ,（159.37±27.99） pg/mL〕较EDSS≤4.5组〔（175.07±92.97） pg/mL ,（217.11±65.34） pg/mL〕患者血清ACTH、CRH水平显著降低（P＝0.001,P＝0.032）。非RRMS组患者血清 ACTH、CRH 水平〔（101.62±57.02） pg/mL ,（174.89±52.48） pg/mL〕与RRMS组〔（172.68±96.11） pg/mL ,（215.61±64.89） pg/mL〕比较均显著下降（P＝0.008,P＝0.032）。结论MS 患者存在HPAA 的功能紊乱。     

短暂性脑缺血发作与IL6、IL8和IL10的关系

目的探讨IL6、IL8及IL10和短暂性脑缺血发作(TIA)患者颈动脉斑块稳定性与疾病预后的关系。方法根据颈动脉CTA检查将TIA患者分为不稳定性斑块组和稳定性斑块组,比较两组患者血清IL6、IL8及IL10水平的差异;检测健康对照组血清IL6、IL8及IL10水平,并与TIA患者组比较;根据TIA患者的预后分为痊愈组、反复发作组、进展为脑梗死组,比较三组患者间血清IL6、IL8及IL10水平的差异。结果不稳定性斑块组患者血清IL6、IL8水平明显高于稳定性斑块组,血清IL10水平低于稳定性斑块组。TIA患者血清IL6、IL8及IL10水平均高于健康对照组。进展为脑梗死组、反复发作组患者的血清IL6、IL8及IL10水平均高于痊愈组。结论血清IL6、IL8水平与颈动脉斑块的稳定性呈负相关,而血清IL10水平与颈动脉斑块的稳定性呈正相关。血清IL6、IL8及IL10水平高的TIA患者易进展为脑梗死。     

灯盏细辛注射液对急性脑梗死患者白细胞介素13及神经功能缺损程度的影响

目的 观察灯盏细辛注射液对急性中度脑梗死患者白细胞介素13（IL-13）及神经功能缺损程度的影响。方法 选择急性中度脑梗死患者102例,随机分灯盏细辛注射液治疗组62例和对照组40例,两组基础治疗相同,对照组用丹参注射液16 ml,治疗组用灯盏细辛注射液40 ml/d,均以14 d为1个疗程,共用2个疗程。比较两组IL-13水平、神经功能缺损程度评分的变化。同期检测30例体检健康者血清IL-13水平。结果 健康者血清IL-13水平（28.7±3.2）ng/L;两组患者血清IL-13水平第7 d时表达最高;第7、14 d,治疗组血清IL-13水平低于对照组[（48.3±5.3）ng/L vs（51.1±3.2）ng/L,P <0.05;（39.8±4.5）ng/L vs（43.7±3.5）ng/L,P<0.01];第14、28d治疗组神经功能缺损程度明显较对照组减轻 （[ 14.9±3.6）分vs（21.4±4.0）分,P <0.01;（12.7±2.7）分vs（15.8±4.1）分,P <0.05]。结论 灯盏细辛注射液可通过抑制急性脑梗死患者的炎症反应,改善患者的预后。     

血清炎性标志物与缺血性脑血管病的关系

目的 比较急性脑梗死、短暂性脑缺血发作(TIA)、陈旧脑梗死患者和健康对照者血清炎性标志物白细胞介素-6(IL-6)、高敏C反应蛋白(hsCRP)、基质金属蛋白酶-9(MMP-9)和组织金属蛋白酶抑制物-1(TIMP-1)水平.方法 收集作者医院急性脑梗死患者56例,TIA患者46例,陈旧脑梗死患者56例,对照组30名,采用ELISA法测定其血IL-6、MMP-9和TIMP-1水平,采用免疫比浊法测定其血hsCRP水平.结果 急性脑梗死和TIA组IL-6水平均高于陈旧脑梗死和对照组 (P<0.05).各组间hsCRP水平比较差异均有统计学意义(P<0.05),水平由高至低依次为急性脑梗死组、TIA组、对照组和陈旧脑梗死组.急性脑梗死组和TIA组MMP-9水平高于陈旧脑梗死和对照组(P<0.05).TIA、急性脑梗死和陈旧脑梗死组TIMP-1水平均高于对照组(P<0.05).IL-6水平(OR=20.525,95%CI:2.623～160.58,P=0.004)和hsCRP(OR=1.878, 95%CI:1.138～3.100, P=0.014)是脑卒中患者预后不佳的独立危险因素.结论 TIA与急性脑梗死患者炎性标志物水平升高,其中IL-6和hsCRP水平升高是患者预后不佳的独立危险因素.     

急性颅脑损伤后血清TNF-α，IL-1，IL-6，IL-8含量变化及其临床意义

目的探讨急性颅脑损伤后血清TNF-α,IL-1,IL-6,IL-8的含量变化及其临床意义。方法用放射免疫法检测50例急性颅脑损伤患者血清IL-1,IL-6,IL-8,TNF-α含量的变化,分析急性颅脑损伤分级与血清中IL-1,IL-6,IL-8,TNF-α含量之间的关系以及其变化趋势。结果重型颅脑损伤组在病程第1、3、7天三个时间点的血清TNF-α,IL-1,IL-6,IL-8的水平较轻、中型组明显升高(P<0.01),IL-6,IL-8早期即有升高,伤后3,7d升高明显,且有继续上升趋势;TNF-α,IL-1分别于伤后第3天达高峰,第7天有所下降,但仍明显高于正常人(P<0.01)。结论血清中TNF-α,IL-1,IL-6,IL-8水平在重型颅脑损伤中明显增高,与颅脑损伤程度呈正相关,并可能在继发性脑损害中起重要作用。     

实验性变态反应性脑脊髓炎IL-10与IL-18的研究

目的研究IL-10与IL-18在实验性变态反应性脑髓炎(EAE)免疫学发病机制中的变化与作用。方法应用豚鼠诱导Wistar大鼠EAE模型,以豚鼠髓鞘碱性蛋白(MBP)与弗氏完全佐剂(CFA)免疫Wistar大鼠,在第11、18、25d处死大鼠,并采用酶联免疫吸附试验(ELISA)测定IL-10与IL-18水平。结果EAE组的IL-10水平在疾病缓解期升高,IL-18的水平随着疾病的进展逐渐升高,在缓解期有所下降,但均显著高于对照组。结论IL-10与IL-18在EAE的免疫学发病机制中具有重要的作用。     

P物质IL-17与IL-6在颅内感染中的表达

目的 探讨P物质、IL-17与IL-6在颅内感染中的表达变化及其相关性.方法 采用酶联免疫吸附试验双抗体夹心法测定23例明确诊断为化脓性脑膜炎与25例明确诊断为病毒性脑炎的患儿入院后24 h内脑脊液中SP、IL-17、IL-6的含量,并与同期入院的非神经系统疾病患儿30例作对照,比较3组SP、IL-17、IL-6水平.结果 脑脊液中SP、IL-17、IL-6变化各组间差异有统计学意义(P<0.05);化脑组升高更显著,与病脑组相比差异有统计学意义(P<0.05).结论 SP、IL-17与IL-6在颅内感染早期表达明显增高,且以细菌感染时升高明显.     

The endocannabinoid anandamide downregulates IL-23 and IL-12 subunits in a viral model of multiple sclerosis: evidence for a cross-talk between IL-12p70/IL-23 axis and IL-10 in microglial cells

Theiler’s virus (TMEV) infection of the central nervous system (CNS) induces an immune-mediated demyelinating disease in susceptible mouse strains and serves as a relevant infection model for human multiple sclerosis (MS). The endocannabinoid system represents a novel therapeutic target for autoimmune and chronic inflammatory diseases due to its anti-inflammatory properties by regulating cytokine network. IL-12p70 and IL-23 are functionally related heterodimeric cytokines that play a crucial role in the pathogenesis of MS. In the present study we showed that the endocannabinoid anandamide (AEA) downregulated the gene expression of IL-12p70 and IL-23 forming subunits mRNAs in the spinal cord of TMEV-infected mice and ameliorated motor disturbances. This was accompanied by significant decreases on the serological levels of IL-12p70/IL-23 and more interestingly, of IL-17A. In contrast, serum levels of IL-10 resulted elevated. In addition, we studied the signalling pathways involved in the regulation of IL-12p70/IL-23 and IL-10 expression in TMEV-infected microglia and addressed the possible interactions of AEA with these pathways. AEA acted through the ERK1/2 and JNK pathways to downregulate IL-12p70 and IL-23 while upregulating IL-10. These effects were partially mediated by CB2 receptor activation. We also described an autocrine circuit of cross-talk between IL-12p70/IL-23 and IL-10, since endogenously produced IL-10 negatively regulates IL-12p70 and IL-23 cytokines in TMEV-infected microglia. This suggests that by altering the cytokine network, AEA could indirectly modify the type of immune responses within the CNS. Accordingly, pharmacological modulation of endocannabinoids might be a useful tool for treating neuroinflammatory diseases.     

Reduced IL-2 but elevated IL-4, IL-6, and IgE serum levels in patients with cerebral infarction during the acute stage

Cytokines in the central nervous system (CNS) may play an important role in functioning as intercellular signals that orchestrate the response to injury. Whether this is a cause or result of the brain disease process is uncertain. We investigated IFN-γ, IL-2, IL-4, IL-6, and IgE in the sera of 38 patients with cerebral infarction during the acute stage and 10 normal controls using an originally devised sensitive sandwich enzyme-linked immunosorbent assay (ELISA). We found that serum levels of IL-2 derived from T helper 1 (Th1) cells were slightly reduced in patients with cerebral infarction, whereas serum levels of IL-4 and IL-6 derived from Th2 cells were elevated significantly. IL-4 induces synthesis of IgE in human B cells. Endogenous IL-6 plays an obligatory role in IL-4-dependent human IgE synthesis. We observed that serum IgE levels were elevated significantly in patients with cerebral infarction. However, serum IFN-γ levels were not elevated significantly in cerebral infarction patients. These findings suggest that elevated IL-4, IL-6, and IgE levels in the human serum may be an important factor in cerebral infarction during the acute stage. Decrease of IL-2 levels in the serum of patients with cerebral infarction may be a regulatory mechanism.     

不同程度颅脑损伤后血清TNF-α、IL-6、IL-8变化及其临床意义

目的 探讨不同程度颅脑损伤病人血清肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）、IL-8水平变化及其临床意义。方法 收集我院2005年4-11月神经外科住院急性颅脑损伤患者41例及对照组25例，对照组清晨空腹抽取静脉血，急性颅脑损伤病人分别在伤后第1、3、7天取外周静脉血3mL。采用放射免疫法检测TNF-α、IL-6、IL-8，分析急性颅脑损伤分级与血清中TNF-α、IL-6、IL-8含量之间的关系及其变化趋势。结果 IL-6、IL-8早期即有升高，伤后3、7d升高显著，且有继续上升趋势；TNF-α于伤后第3天达高峰，第7天有所下降，但仍显著高于对照组。重型颅脑损伤组在病程第1、3、7天三个时间点的血清TNF-α、IL-6、IL-8的水平较轻、中型组显著升高（P〈0．05）。结论 血清中TNF-α、IL-6、IL-8参与了急性颅脑损伤的病理生理过程，其水平在重型颅脑损伤中显著增高，与颅脑损伤程度呈正相关，并可能在继发性脑损害中起重要作用。其测定对于早期评估颅脑损伤的严重程度和预后有重要的临床意义。     

亚低温对外伤性蛛网膜下腔出血患者脑脊液中TNF-α、IL-1和IL-6的影响

目的研究亚低温对外伤性蛛网膜下腔出血脑脊液中TNF-α、IL-1和IL-6的影响,以进一步探讨亚低温对颅脑损伤的治疗作用。方法外伤性蛛网膜下腔出血患者32人,男性23人,女性9人,年龄17~56岁,平均年龄33±7岁,Glasgow分级9±4。分为亚低温组19人,对照组13人。标本采集,患者每天腰穿一次,留取中段脑脊液2ml。立即送实验室检测,TNF-α浓度采用放免法测定,γ放免计数仪检测。IL-1,IL-6浓度采用酶联免疫吸附法测定。结果亚低温组脑脊液TNF-α、IL-1和IL-6浓度除第1天和对照组无明显差异外,其余以后各天均明显增高(P<0.05).结论亚低温可以通过降低脑脊液内TNF、IL-1和IL-6的浓度,参与对外伤性蛛网膜下腔出血的有益治疗作用。     

蛛网膜下腔出血对坐骨神经TNF-α、IL-1β、IL-6表达的影响

目的观察TNF-α、IL-1β、IL-6在坐骨神经上的表达变化。方法制作SD大鼠蛛网膜下腔出血模型,分别在3、7、14d取坐骨神经进行TNF-α、IL-1β、IL-6免疫组化与荧光染色,并对结果进行数据分析。结果蛛网膜下腔出血模型的坐骨神经的TNFα-、IL-1β和IL-6表达较对照组高(P<0.05),3、7d明显升高,14d有所下降但仍高于对照组。结论蛛网膜下腔出血后,坐骨神经TNF-α、IL-1β、IL-6表达升高。     

Low serum IL-10 concentrations and loss of regulatory association between IL-6 and IL-10 in adults with major depression

Elevated circulating pro-inflammatory cytokines are associated with symptoms of depression, and disorders involving chronic inflammation are often co-morbid with major depression. Since healthy immune regulation is accomplished through counter-balancing effects of pro- and anti-inflammatory cytokines, we hypothesized that depressed subjects (compared to controls) would express lower concentrations of the anti-inflammatory/immunoregulatory cytokine interleukin (IL)-10, and a higher IL-6/IL-10 ratio. We also examined the possibility that depressed subjects may exhibit a deficiency in the regulatory loop involving IL-6 induced secretion of IL-10. Therefore, we hypothesized that circulating IL-6 and IL-10 would be positively correlated in controls, while the correlation would be weaker in depressed subjects. Resting state serum cytokine concentrations were quantified in 12 unmedicated depressed subjects, and 11 age, gender, and ethnicity-matched controls. Depressed subjects showed significantly lower IL-10 (p = 0.03, Cohen’s d = −0.96), non-significantly higher IL-6, and significantly higher IL-6/IL-10 ratios (p = 0.05, Cohen’s d = 0.50). Across all participants, higher scores on the self-rated Inventory of Depressive Symptoms were associated with lower IL-10 (r(21) = −0.57, p = 0.005) and non-significantly higher IL-6/IL-10 ratios (r(21) = 0.38, p = 0.07), but not related to IL-6 concentrations. As hypothesized, IL-6 and IL-10 concentrations were strongly and positively correlated in controls (r(9) = 0.81, p = 0.003), but were completely dissociated in depressed subjects (r(10) = 0.01, p = 0.98). These results suggest that lower IL-10 levels, a higher IL-6/IL-10 ratio, and the apparent absence of a counter-balancing, immunoregulatory increase in IL-10 in response to elevated IL-6 concentrations contribute to the pro-inflammatory physiological milieu that is known to be associated with major depression. Therefore, reduced induction/availability of IL-10, that would normally inhibit pro-inflammatory cytokine actions and resolve inflammation, may contribute to the depressogenic as well as the inflammatory disease-promoting effects of chronic, low-level elevations in pro-inflammatory cytokines.     

白细胞介素18在脑肿瘤中的研究进展

IL-18是一种Th1细胞因子,它能高水平诱生IFN-,增强NK细胞活性,显著增强TH1型免疫反应,调节各种细胞因子的生成,具有明显的抗肿瘤功能。本文主要就IL-18的来源、生物学功能及抗脑肿瘤研究进展作一介绍。