哮喘气道炎症粘附机制的实验研究

目的：评价细胞间粘附分子１（ＩＣＡＭ－１）、Ｐ选择素在哮喘气道炎症粘附机制中的作用,进一步阐明哮喘的发病机理。方法：用酶联免疫吸附试验、肺组织免疫组化检查和呼吸生理学方法系统观察正常组和哮喘组豚鼠各项指标。结果：（１）哮喘组豚鼠肺潮气量、动态肺顺应性（Ｃｄｙｎ）和肺气道阻力与对照组比较差异有显著性（Ｐ＜０．０１及Ｐ＜０．０５）。（２）哮喘组豚鼠血浆和肺泡灌洗液（ＢＡＬＦ）可溶性ＩＣＡＭ－１（ｓＩＣＡＭ－１）、可溶性Ｐ选择素、血清和ＢＡＬＦ嗜酸粒细胞阳离子蛋白（ＥＣＰ）与对照组比较,差异有显著性（Ｐ＜０．０１）;ＢＡＬＦ中白细胞介素８（ＩＬ－８）与对照组比较差异也有显著性（Ｐ＜０．０１）。（３）哮喘组豚鼠肺组织（气道上皮和血管内皮）ＩＣＡＭ－１和ＩＬ－８表达与对照组比较,差异有显著性（Ｐ＜０．０１）。结论：ＩＣＡＭ－１、Ｐ选择素、ＩＬ－８、ＥＣＰ参与介导了哮喘气道炎症的粘附过程。     

银屑病患者T淋巴细胞集落形成及IL－2R的研究

２１例银屑病患者及１０例正常人外周血Ｔ淋巴细胞集落形成单位（ＴＬ－ＣＦＵ）及白细胞介素２受体（ＩＬ－２Ｒ）表达检测结果显示，银屑病患者ＴＬ－ＣＦＵ数及ＩＬ－２Ｒ表达均低于正常人（Ｐ均＜０．０１），且进行期低于静止期（Ｐ＜０．０１，Ｐ＜０．０１）。寻常型与脓疤型比较均无明显差异（Ｐ均＞０．０５）。ＩＬ－２Ｒ表达与ＴＬ－ＣＦＵ数呈正相关（Ｐ＜０．０１）。表明银屑病患者细胞免疫功能低下，且Ｔ细胞免疫功能在祖细胞水平即有损害     

哮喘患儿IL—12,IL—13与总IgE水平变化

目的：探讨哮喘患儿白细胞介素１２（ＩＬ－１２）、白细胞介素１３（ＩＬ－１３）与总免疫球蛋白Ｅ（总ＩｇＥ）的变化。方法：取静脉血,用ＥＬＩＳＡ方法检测ＩＬ－１２、ＩＬ－１３与总ＩｇＥ水平,并对检测结果进行统计学处理。结果：发作期哮喘患儿血浆及外周血单个核细胞（ＰＢＭＣ）诱生的ＩＬ－１２水平显著低于哮喘缓解组,Ｐ〈０．０１;两组均显著低于正常对照组,Ｐ〈０．０１;发作期ＩＬ－１３水平显著高于缓解组,Ｐ     

Graves病淋巴细胞白介素2受体及转铁蛋白受体的表达

应用卵白素·生物素·过氧化物酶复合物（ＡＢＣ）法检测５４例Ｇｒａｖｅｓ病患者外周血淋巴细胞ＩＬ－２Ｒ，ＣＤ２５及ＴｆＲ，ＣＤ７１的表达。结果表明，Ｇｒａｖｅｓ病亢进期患者ＩＬ－２Ｒ与ＴｆＲ均显著高于正常对照组（Ｐ＜０．００１），缓解期ＩＬ－２Ｒ及ＴｆＲ迅速恢复（与亢进期比，Ｐ＜０．００１），但ＩＬ－２Ｒ仍高于正常对照组（Ｐ＜０．００１），而ＴｆＲ与正常对照组差异无显著性（Ｐ＞０．０５），ＩＬ－２Ｒ与Ｔ３（ｒ＝０．５８６８，Ｐ＜０．０１），Ｔ４（ｒ＝０．４９８５，Ｐ＜０．０１）呈正相关，ＴｆＲ与Ｔ３（ｒ＝０．４８５２，Ｐ＜０．０１），Ｔ４（ｒ＝０．４２３８，Ｐ＜０．０１）呈正相关，并对Ｇｒａｖｅｓ病出现ＩＬ－２Ｒ及ＴｆＲ变化的意义进行了讨论     

支气管哮喘患者外周血白细胞糖皮质激素受体的改变

应用放射配体结合法和放射免疫法分别检测了１７例哮喘患发作期外周血白细胞糖皮质激素受体（ＧＲ）和血浆皮质醇（Ｆ）。结果：外周血白细胞ＧＲ最大结合容量（Ｒ０）为１２９０８±２５０１位点／细胞，与健康对照组比较无显差异（Ｐ＞０．０５）。ＧＲ平衡解离常数（Ｋｄ）为１６．５４±５．３６ｎｍｏｌ／Ｌ，明显高于对照组（Ｐ＜０．０１）。血浆Ｆ为４３２±２７５ｎｍｏｌ／Ｌ，与对照组比较无显差异（Ｐ＞０．０５）     

自然流产与EGF,GM—CSF及sIL—6R的关系探讨

目的 探讨ＥＧＦ、ＧＭ－ＣＳＦ及ｓＩＬ－６Ｒ在自然流产中的作用。方法 用酶联免疫吸附实验（ＥＬＩＳＡ）方法测定血清中３种细胞因子的浓度。结果 Ａ组（自然流产组）血清中ＥＧＦ浓度明显低于Ｂ组（正常早孕组）（Ｐ〈０．０１）,但与Ｃ组（健康非孕组）差异不显。Ａ组血清中ＧＭ－ＣＳＦ浓度明显低于Ｂ组（Ｐ〈０．０１）,但较Ｃ组高（Ｐ〈０．０５）。Ａ组血清中ｓＩＬ－６Ｒ浓度明显低于Ｂ和Ｃ组（Ｐ〈０．０１）,而     

肺癌患者外周血单个核细胞分泌白细胞介素－2受体的研究

采用ＥＬＩＳＡ法对３３例肺癌和２８例健康人外周血单个核细胞（ＰＢＭＣ）分泌可溶性白细胞介素－２受体（ｓＩＬ－２Ｒ）能力的研究显示：肺癌患者ＰＢＭＣ分泌；ＩＬ－２Ｒ能力明显高于健康人（Ｐ＜０．０１）。但鳞癌、腺癌、小细胞未分化癌之间，ＰＢＭＣ分泌ｓＩＬ－２Ｒ能力无差别，三者分别较健康人显著增高（Ｐ＜０．０１）。在肺癌Ⅰ、Ⅱ、Ⅲ、Ⅳ期之间，ＰＢＭＣ分泌ｓＩＬ－２Ｒ能力亦无显著性差异。     

银屑病患者T淋巴细胞集落形成及IL—2R的研究

２１例银屑病患者及１０例正常人外周血Ｔ淋巴细胞集落形成单位（ＴＬ－ＣＦＵ）及白细胞介素２受体（ＩＬ－２Ｒ）表达检测结果显示，银屑病患者ＴＬ＿ＣＦＵ数及ＩＬ－２Ｒ表达均低于正常人（Ｐ均〈０．０１），且进行期低于静止期（Ｐ〈０．０１，Ｐ〈０．０１）。寻常型与脓疱型比较均无明显差异（Ｐ均〉０．０５）。ＩＬ－２Ｒ表达与ＴＬ－ＣＦＵ数呈正相关（Ｐ〈０．０１）。表明银屑病患者细胞免疫功能低下，且Ｔ细胞免疫功能     

哮喘中外周血单个核细胞白细胞介素5表达及意义研究

该文研究了哮喘豚鼠嗜酸性粒细胞（ＥＯＳ）在外周血及支气管肺泡灌洗液（ＢＡＬＦ）中的变化,用ＲＴ－ＰＣＲ半定量测定了外周血单个核细胞（ＰＢＭＣ）及支气管组织白细胞介素５（ＩＬ－５）ｍＲＮＡ表达量。结晶显示哮喘豚鼠ＥＯＳ及ＩＬ－５ｍＲＮＡ表达量均较对照组及地塞米松干预组显著升高,ＰＢＭＣ中ＩＬ－５ｍＲＮＡ表达量与支这组织ＩＬ－５表达及外周血ＥＯＳ计数成正相关。提示哮喘豚鼠ＰＢＭＣ、ＩＬ－５ｍＲＮＡ表达     

急性颅脑损伤患者脑脊液中髓鞘碱蛋白的变化及其意义

目的：为探讨急性颅脑损伤患者脑脊液（ＣＳＦ）中髓鞘碱蛋白（ＭＢＰ）的变化及意义。方法：用放射免疫分析法测定３４例急性颅脑损伤组患者ＣＳＦ中ＭＢＰ。结果：ＣＳＦ中ＭＢＰ在急性颅脑损伤组明显高于对照组（Ｐ＜０．０１）,在ＡＤＣＩ患者明显高于ＡＬＣＩ患者（Ｐ＜０．０１）;ＡＤＣＩ患者入院时ＧＣＳ明显低于ＡＬＣＩ患者,而ＧＯＳ明显差于ＡＬＣＩ患者（Ｐ＜０．０１）;ＭＢＰ与ＧＣＳ和ＧＯＳ均呈明显负相关（ｒ＝－０．６１２,ｒ＝－０．５９８,Ｐ＜０．０１）。结论：急性颅脑损伤患者ＣＳＦ中ＭＢＰ升高,测定ＣＳＦ中ＭＢＰ有助于估计急性颅脑损伤患者病情轻重及预后;有助于ＡＤＣＩ的诊断。     

Expression and significance of myeloid differentiation factor 88 in marrow dendritic cells in asthmatic rats with cigarette smoke exposure

Background  Smoking causes frequent asthma attacks, leading to a rapid decline in lung function in patients with asthma, and it can also reduce the therapeutic effect of glucocorticoids in patients with asthma. Therefore, the present study aimed to investigate the effect of cigarette smoke on the expression of myeloid differentiation factor 88 (MyD88) in marrow dendritic cells (DCs) in asthmatic rats, and to explore the molecular mechanism of cigarette smoke exposure on asthma by DCs.

Methods  Forty Wistar rats were randomly divided into the following groups: control, smoke exposure, asthma, and asthma combined with smoke exposure. The animal model was established, and then rat bone marrow-derived DCs were collected. Additionally, rat spleen lymphocytes and bone marrow-derived DCs were cultured together for mixed lymphocyte responses. Interferon (IFN)-gamma and interleukin (IL)-4, IL-10, and IL-12 expressions were determined by enzyme-linked immunosorbent assay (ELISA). MyD88 expression was determined by Western blotting. The proliferation of lymphocytes was examined with methyl thiazolyl tetrazolium (MTT) colorimetric assay.

Results  MyD88 expression was decreased in the asthma combined with smoke exposure group compared to the asthma group (P <0.01), and IL-10 and IL-12 expressions were decreased in the asthma combined with smoke exposure group compared to control group (P <0.01). In addition, DCs stimulating activity on allogeneic lymphocytes were significantly decreased in the smoke exposure combined with asthma group compared to the control and asthma groups (P <0.01). After allogeneic mixed lymphocyte responses, IL-4 expression was increased and IFN-gamma was decreased in the asthma group and the asthma combined with smoke exposure group compared to control group (P <0.01). IL-4 expression was increased and IFN-gamma was decreased in the asthma combined with smoke exposure group compared to the asthma group (P <0.01). The study also showed that MyD88 expression was positively correlated with IL-12 and IFN-gamma expressions and the activity of lymphocytes (P <0.01), and negatively correlated with IL-4 expression (P <0.01).

Conclusions  Smoking aggravates asthma by weankening immunological mechanism. MyD88-dependent pathways may play a role in the immunological balance and activation of lymphocytes.

     

细胞因子和IgE检测在支气管哮喘诊断中的价值

目的探讨支气管哮喘患者血清白细胞介素一6（IL-6）、白细胞介素一10（IL-10）、白细胞介素-16（IL-16）和免疫球蛋白IgE的动态变化和检测的临床意义。方法收集30例支气管哮喘发作期患者（哮喘组）和30例正常对照者（对照组）的血清,采用酶联免疫吸附试验（ELISA）测定血清中IL-6、IL-10、IL-16和总IgE。结果与正常对照组比较,哮喘组血清IL-6、IL-16和总IgE水平明显增高,相比较有显著性差异（P〈0．05）;而IL-10水平明显降低,相比较有显著性差异（P〈0．05）;哮喘组总IgE与IL-6、IL-16之间呈正相关（r=0．6871,r=0．8633,P〈0．01）;与IL-10之间存在负相关（r=-0．4782,P〈0．01）。结论IL-6、IL-10、IL-16和总IgE与哮喘发病机制有关,动态测定这些指标有助于病情评估。     

血红素氧化酶-1在前列腺的表达及雄激素和雌激素对其表达的影响

目的 观察雄激素和雌激素去势后大鼠前列腺腹侧叶中血红素氧化酶－1（HO－1）基因表达的影响。方法 采用睾丸切除术创建大鼠去势模型，用RT－PCR方法观察HO－1的转录水平，应用免疫组织化学结合图像分析技术，观察去势，外源性雄激素和雌激素对大鼠前列腺腹侧叶中HO－1蛋白水平及分布的影响。结果 去势组HO－1 mRNA转录水平和HO－1蛋白表达水平显著低于正常对照组（P＜0．01）；外源性给予雄激素组和雌激素组HO－1 mRNA表达水平和HO－1蛋白表达水平明显增高（P＜0．01），且雌激素引起前列腺间质HO－1表达增加。结论 一氧化碳－血红素氧化酶系统可能参与了雌、雄激素引起前列腺异常增殖的病理过程。     

白三烯受体拮抗剂对哮喘局部免疫影响的实验研究

目的为研究白三烯(LTs)拮抗剂安可来(Accolate)对哮喘大鼠气道嗜酸性粒细胞(EOS)、淋巴细胞(Lym)浸润以及T细胞活化表达白细胞介素-2受体(IL-2R)的影响,探讨安可来治疗哮喘的作用机制.方法应用卵清蛋白腹腔注射致敏和反复超声雾化吸入激发诱喘建立大鼠哮喘模型.随机分为正常对照组(A组)、阳性对照组(B组)、预防治疗组(C组)和治疗组(D组).A组以生理盐水致敏和激发,B、C、D组建立哮喘模型.C组自激发诱喘前1周起预防性给予安可来饲喂,诱喘期继续治疗.D组自激发日起行安可来饲喂.病理切片观察大鼠支气管壁EOS、Lym浸润,ABC法检测大鼠T细胞IL-2R的表达.结果正常对照组大鼠支气管壁可见少量Lym浸润但无明显EOS浸润和炎症反应,IL-2R阳性细胞数目很少.阳性对照组支气管壁EOS、Lym浸润以及IL-2R阳性细胞数目明显增多,较正常对照组有显著差异(P＜0.01).饲喂安可来预防和(或)治疗能减少支气管壁EOS、Lym浸润以及IL-2R阳性细胞数目,与阳性对照组相比有显著差异(P＜0.05).结论安可来能减轻哮喘大鼠肺组织炎症反应,抑制EOS、Lym等炎症细胞向气道组织的浸润,对大鼠T细胞活化表达IL-2R亦有明显抑制作用.     

化痰祛瘀疏肝法对哮喘小鼠IL-13/IL-18失衡的干预作用

目的探讨化痰祛瘀疏肝法对哮喘小鼠白介素13、18(IL-13/IL-18)失衡的干预作用。方法以10%卵蛋白/氢氧化铝[OVA/AL(OH)3]致敏、5%卵蛋白激发复制支气管哮喘小鼠模型,于实验第16～43 d给药,第44 d取材。用酶联免疫试验(ELISA)法检测肺泡灌洗液(BALF)中IL-13、IL-18浓度,实时定量PCR(RT-PCR)法检测肺组织匀浆中IL-13、IL-18 mRNA表达。结果模型组小鼠IL-13浓度及mRNA均较空白组显著升高(P<0.01);IL-18浓度及mRNA均较空白组显著降低(P<0.05);各处理组IL-13浓度及mRNA均较模型组显著降低(P<0.01),IL-18浓度及mRNA均显著升高(P<0.05);PCF组、SGPCG组IL-13浓度降低不及地米组(P<0.01),PCF组、SGPCG组IL-18 mRNA、IL-13/IL-18比值均与地米组相似(P>0.05);PCF组、SGPCG组间IL-13、IL-18浓度及mRNA、IL-13/IL-18比值差异均无统计学意义(P>0.05)。结论化痰祛瘀疏肝法对哮喘小鼠升高的IL-13浓度及mRNA均有降低作用,对其降低的IL-18浓度及mRNA均有升高作用,对IL-13/IL-18比值的调节总体与地塞米松和化痰祛瘀平喘法相似。提示化痰祛瘀疏肝法对哮喘小鼠神经源性炎症相关的Th1/Th2免疫失衡有较为确切的干预作用。     

局灶性脑缺血再灌注大鼠IL—1Ra mRNA的表达

目的　观察脑缺血再灌注后白细胞介素 1受体拮抗剂 (IL 1Ra)mRNA的表达。②方法　采用线栓法制备SD大鼠局灶性大脑中动脉阻塞 (MCAO)动物模型 ,应用RT PCR方法观察脑缺血再灌注对大鼠IL 1RamRNA表达的影响。③结果　MCAO模型大鼠缺血侧大脑皮质再灌注后 12 ,2 4h的IL 1RamRNA表达与正常对照组比较明显增加 (F =39.84,q=9.0 3,15 .91,P <0 .0 0 1) ;缺血侧纹状体缺血再灌注后 12h的IL 1RamRNA表达与正常对照组比较明显增加 (F =7.37,q=6 .5 4,P <0 .0 0 1)。④结论　脑缺血后内源性IL 1RamRNA表达增加 ,可能是机体对缺血性损伤的自我保护机制。     

Impact of psychosocial stress on airway inflammation and its mechanism in a murine model of allergic asthma

Background  It has already been recognized that psychosocial stress evokes asthma exacerbation; however, the mechanism of how stress gets inside the body is not clear. This study aimed to observe the impact of psychosocial stress on airway inflammation and its mechanism in the ovalbumin-induced asthmatic mice combined with social disruption stress.

Methods  Thirty-six male BALB/c mice were randomly divided into: control group, asthma group (ovalbumin-induced), asthma plus social disruption stress group (SDR), and SDR group. The open field video tracking system was used to assess animal behaviors. The invasive pulmonary resistance (RL) and dynamic lung compliance (cdyn) test system from Buxco was applied to detect pulmonary function. The enzyme-linked immunosorbent assay (ELISA) was utilized to determine OVA-IgE, T-helper type 2 (Th2) cytokines (IL-4, IL-5, IL-13) and corticosterone in mouse serum, the Th2 cytokines (IL-4, IL-5, IL-13, IL-6, TNF-α) in bronchoalveolar lavage fluid (BALF), and IL-6 and TNF-α levels in the supernatant of splenocytes cultured in vitro. Hematoxylin-eosin (H&E) staining was used to assess airway inflammation in lung histology. The cell count kit-8 assay (CCK-8) was applied to evaluate the inhibitory effect of corticosterone on splenocyte proliferation induced by lipopolysaccharide (LPS). Real time-PCR and Western blotting were utilized to determine glucocorticoid receptor (GR) mRNA and GR protein expression in lungs.

Results  The open field test showed that combined allergen exposure and repeated stress significantly shortened the time the mice spent in the center of the open field (P <0.01), increased ambulatory activity (P <0.01) and the count of fecal boli (P <0.01), but deceased vertical activity (P <0.01). Results from pulmonary function demonstrated that airway hyperresponsiveness (AHR) was enhanced by psychosocial stress compared with allergy exposure alone. The ELISA results showed that cytokines in serum and BALF were significantly increased (P <0.05). Moreover, the lung histology showed that infiltrated inflammatory cells were significantly increased in the asthma-SDR group compared with the asthma group (P <0.05). Interestingly, serum corticosterone was remarkably raised by psychosocial stress (P <0.05). In addition, the inhibitory effect of corticosterone on IL-6 and TNF-α in LPS-stimulated splenocyte cultures in vitro was diminished in the asthma-SDR group compared to the asthma group. The CCK-8 test revealed that the inhibition effect of corticosterone on splenocyte proliferation induced by LPS was significantly impaired in the SDR and asthma-SDR groups, while no significant effect was observed in the control and asthma groups. Furthermore, expression of GR mRNA and GR protein were significantly reduced in the lung tissues of the asthma-SDR group (P <0.05).

Conclusions  Social disruption stress can promote anxiety behavior, activate the hypothalamic-pituitary-adrenal (HPA) axis, increase AHR and inflammation, and also impair glucocorticoid sensitivity and its function in a murine model of asthma. The down-regulation of GR expression induced by social disruption stress is in part associated with glucocorticoid insensitivity, which leads to asthma exacerbation.

     

哮喘小鼠模型中IL-25表达及其对肥大细胞IL-6分泌的影响

目的:探讨哮喘小鼠模型中白细胞介素(interleukin,IL)-25的表达,研究其对肥大细胞IL-6分泌的影响?方法:6~8周龄BALB/c小鼠随机分为对照组和哮喘组,分别用等量磷酸盐缓冲液(phosphate buffer solution,PBS)或卵清蛋白(ovalbumin,OVA)致敏,检测肺泡灌洗液(bronchoalveolar lavage fluid,BALF)中细胞总数及嗜酸性粒细胞(eosnophils,EOS)计数验证模型的成功建立?两组小鼠肺组织中IL-25 mRNA?BALF及血清中IL-25的表达分别应用逆转录-聚合酶链反应法?酶联免疫吸附实验(enzyme-linked immunosorbent assay,ELISA)检测?小鼠肥大细胞P815分为对照组和IL-25组,分别予等量培养基和IL-25干预,收集细胞培养上清,用ELISA检测IL-6的水平?结果:哮喘组BALF中细胞总数及EOS计数较对照组显著升高(P < 0.01),小鼠出现呼吸频率加快?烦躁不安等表现,模型建立成功?哮喘组肺组织中IL-25 mRNA?BALF及血清中IL-25表达较正常组显著升高(P < 0.01)?细胞水平的研究发现IL-25组P815上清中IL-6表达较对照组显著升高(P < 0.01)?结论:IL-25在OVA诱导哮喘小鼠模型中表达升高?IL-25刺激肥大细胞分泌IL-6,可能在哮喘的发病中起促进作用?     

益气补肾方药对肾虚小鼠细胞因子IL-1、IL-2及IL-12基因表达的影响

目的　探讨益气补肾中药对醋酸可的松致肾虚小鼠腹腔巨噬细胞IL 1及脾脏细胞因子IL 2、IL 12活性及脾脏IL 1、IL 2、IL 12mRNA表达的影响。方法　用醋酸可的松制备肾虚动物模型 ,经益气补肾方药灌胃给药 6周后 ,生物学方法观察腹腔巨噬细胞IL 1、脾脏淋巴细胞IL 2、IL 12的活性水平 ,RT PCR方法观察脾脏IL 1、IL 2及IL 12mRNA的表达。结果　模型动物IL 1、IL 2及IL 12的活性水平较正常小鼠下降 ,其mRNA表达均受到抑制 ,与正常对照组比差异显著 (P <0 0 5 ) ;经益气补肾方药治疗后 ,三种细胞因子活性水平及其mRNA表达均有不同程度的提高。结论　益气补肾方药可能是改善外源糖皮质激素所致肾虚及由此而导致的免疫衰老较理想的方法     

新生儿低氧缺血性脑病Th2细胞功能的检测

①目的了解低氧缺血性脑病(HIE)新生儿Th2细胞功能变化及其与HIE间的关系.②方法采用ELISA法和单克隆抗体间接免疫荧光法,检测46例HIE病儿不同病期血浆和外周血单个核细胞(PBMC)体外产生白细胞介素(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检测结果进行对照.③结果 HIE病程第1天(D1)血浆及PBMC体外产生IL-6,IL-8和IL-10水平明显高于正常对照组(z=4.653～5.856,P<0.01);中重度及并发多器官功能障碍综合征(MODS)的HIE病儿血浆及PBMC体外产生IL-6,IL-8水平分别高于轻度及无MODS病儿(z=2.228～2.701,P<0.05;z=2.877～4.187,P<0.01),而IL-10水平无显著性差异(z=0.450～1.850,P>0.05);T细胞IL-2R表达率明显低于正常对照组(t=3.561,P<0.01),中重度HIE病儿尤著(t′=4.194,P<0.01).血浆IL-6,IL-8,IL-10水平间呈显著正相关(r=0.629～0.746,P<0.01);血浆及PBMC体外产生IL-6,IL-8水平与血清脑型磷酸激酶水平呈显著正相关(r=0.489～0.691,P<0.05,0.01),与T细胞IL-2R表达率呈显著负相关(r=-0.394～-0.451,P<0.05,0.01).病程第3天(D3)时血浆和PBMC体外产生IL-6,IL-8和IL-10水平较D1时皆无显著性差异(z=0.314～1.371,P>0.05);临床症状消失时(D7)血浆IL-6,IL-8水平均明显低于D1和D3时(z=2.455,P<0.05;z=2.725～3.856,P<0.01),而血浆IL-10水平虽较D1和D3时降低但差异无显著性(z=1.437,1.248,P>0.05).④结论 HIE时血浆中和PBMC体外产生IL-6,IL-8和IL-10水平明显增高,提示Th2细胞功能异常,此在HIE的发病机制中起重要作用.