缺氧缺血性脑病新生儿血清脂联素、白细胞介素-6变化的意义

目的探讨不同时期HIE新生儿血清脂联素与IL-6水平和其相关性，及其与HIE临床分度的关系。方法采用ELISA法对58例HIE患儿（HIE组）及26例非HIE新生儿（对照组）血清脂联素与IL-6水平进行动态检测，并对检测结果采用SPSS 10．0软件进行统计学处理。结果中、重度HIE组急性期血清脂联素水平与轻度组及对照组比较均明湿下降（Pa〈0．001），重度组较中度组明显下降（P〈0．001）；恢复期，中、重度组血清脂联素水平仍明显低于轻度HIE及对照组（Pa〈0．001），重度组明显低于中度组（P〈0．01）；急性期，中、重度HIE患儿血清脂联素水平降低，与恢复期比较均有差异性显著（Pa〈0．001），轻度HIE组和对照组血清脂联素水平在急性期和恢复期比较差异均无统计学意义（Pa〉0．05）。中、重度组HIE患儿急性期血清IL-6水平与对照组及轻度组比较均明显升高（Pa〈0．001），重度组与中度组比较亦明显升高（P〈0．001）；恢复期，中、重度组血清IL-6水平仍明显高于轻度HIE及对照组（Pa〈0．001），重度组明显高于中度组（P〈0．001）；急性期，中、重度HIE患儿血清IL-6水平升高，均明显高于恢复期（Pa〈0．001），轻度HIE组和对照组患儿血清IL-6水平在急性期和恢复期比较差异均无统计学意义（Pa〉0．05）。HIE患儿血清脂联素与IL-6水平呈显著负相关（r=-0．852 P〈0．001）。结论检测血清脂联素和IL-6水平可作为临床HIE病情程度的判断指标之一，对临床诊断及预后的判断具有指导意义。     

急性病毒性心肌炎患儿血清肿瘤坏死因子-α、白细胞介素-6水平变化的意义

目的探讨急性病毒性心肌炎（AVM）患儿血清肿瘤坏死因子-α（TNF-α）及白细胞介素-6（IL-6）水平变化的意义。方法应用放射免疫法（RIA）和酶联免疫吸附法（ELISA）检测53例AVM患儿及20例健康儿童血清TNF-α及IL-6水平,分析TNF-α及IL-6血清水平与儿童AVM发生的关系。结果AVM组急性期血清TNF-α和IL-6水平分别为（526.7±32.9）和（3.23±0.53）mg/L,健康对照组分别为（383.1±27.5）和（1.63±0.22）mg/L,二组比较均有显著性差异（Pa〈0.05）;临床治愈后,AVM组TNF-α及IL-6分别降至（407.3±34.4）和（1.97±0.29）mg/L,与健康对照组比较均无显著性差异（Pa〉0.05）。结论AVM患儿急性期血清TNF-α和IL-6明显增高,心肌炎治愈后降至正常,检测TNF-α及IL-6血清水平及变化有助于判断AVM患儿病情及心肌损害程度。     

肺炎支原体肺炎患儿血清白细胞介素-10、转化生长因子-β1检测的意义

目的探讨肺炎支原体肺炎（MPP）患儿急性期及恢复期外周血IL-10、转化生长因子-β1（TGFβ-1）水平变化的临床意义。方法采用双抗体夹心酶联免疫吸附法（ELISA）测定26例MPP急性期和其中恢复期9例患儿及12例健康儿童血清IL-10、TGFβ-1水平。比较MPP急性期与恢复期IL-10、TGFβ-1的差异。结果MPP急性期及恢复期患儿血清IL-10水平均显著低于对照组（P〈0.01,0.05）,急性期及恢复期MPP患儿血清TGFβ-1均明显高于对照组（Pa〈0.01）。MPP患儿急性期与恢复期IL-10、TGFβ-1无明显差异（Pa〉0.05）。结论IL-10低水平表达与MPP发病可能有关,存在炎症反应失控,同时存在以TGFβ-1高水平表达的抗感染反应占优势。     

过敏性紫癜肾炎患儿血清细胞因子水平变化及意义

目的 了解过敏性紫癜肾炎（HSPN）患儿血清白细胞介素2、4、10（IL-2、4、10）及肿瘤坏死因子α（TNF—α）的水平变化及其与血IgA、IgG、IgM、IgE、尿红细胞计数的关系,初步探讨细胞因子在HSPN发病中的作用及其机制。方法 采用ELISA法检测42例HSPN患儿及42例健康儿童的血清IL-2、IL-4、IL-10、TNF—α的含量,采用速率散射比浊法检测血IgA、IgG、IgM、IgE含量。结果 HSPN组血清IL-4、IL-10、TNF—α含量高于对照组（P〈0．05）,IL-2含量低于对照组（P〈0．05）;血IgA、IgE水平高于对照组（P〈0．05）,IgG、IgM水平与对照组相比差异无显著性（P〉0．05）;IL-10水平与IgA呈正相关（r=0．4066,P〈0．05）,IL-4水平与IgE呈正相关（r=0．5281,P〈0.05）;IL-2与尿红细胞计数呈负相关（r=-0．6187,P〈0．05）,TNF—α与尿红细胞计数呈正相关（r=0．7033,P〈0．05）。结论 血清IL-2、IL-4、IL-10、TNF-α、IgA、IgE与HSPN的发病过程密切相关,同时存在着细胞免疫与体液免疫功能的紊乱;IL-2和TNF—α在HSPN的发病中起相反作用,检测IL-2和TNF—α水平可作为初步估测HSPN患儿肾损害程度及预后的指标。     

川崎病患儿白细胞介素-15水平变化的临床意义

目的探讨白细胞介素-15（IL-15）在川崎病（KD）发病机制中的作用及其应用价值。方法选择2004年10月～2006年1月本院住院的30例KD患儿作为研究对象,采用酶联免疫吸附法（ELISA）检测KD患儿急性期和恢复期血清IL-15水平,同期检测30例下呼吸道感染发热期和20例正常健康儿童作为对照。结果急性期KD患儿血清IL-15水平明显高于健康对照组,二者比较有显著性差异（q=25.64P〈0.01）;恢复期KD患儿血清IL-15水平下降,但仍较健康对照组增高,二者比较有显著性差异（q=4.00P〈0.01）;KD患儿血清IL-15水平急性期与恢复期比较有显著性差异（t=14.87P〈0.01）。KD患儿急性期和恢复期血清IL-15水平均明显高于下呼吸道感染患儿急性期和恢复期,有显著性差异（急性期t=6.28P〈0.01;恢复期t=4.34P〈0.01）;急性期随KD患儿IL-15水平升高,ESR也相应升高,二者呈显著正相关（r=0.371P=0.044）,但与外周血WBC计数、CRP和血清清蛋白（ALB）变化无明显相关性;与IgG存在正相关性（r=0.372P=0.043）。结论IL-15参与KD的病理生理过程,IL-15可能促使免疫细胞大量激活,进而介导组织免疫病理损伤。IL-15水平变化反映KD的病情状况,可能为早期诊断提供一定线索。     

肺炎支原体肺炎患儿血清白细胞介素-6及可溶性白细胞介素-6受体活性变化及意义

目的：为正确认识肺炎支原体肺炎(MPP)患儿免疫状态，该研究检测了MPP和非肺炎支原体肺炎患儿血清白细胞介素6(IL6)及可溶性白细胞介素6受体(sIL6R)的变化，探讨其对MPP和非MPP患儿病情的影响，并为选择合理的MPP治疗手段提供理论依据。方法：用ELISA法检测MPP患儿(n=41)及非MPP患儿(n=20)急性期和恢复期血清IL-6及sIL-6R含量。结果：①MPP 患儿血清IL-6急性期和恢复期分别为 2.01±0.41，1.12±0.67 ng/L；sIL-6R急性期和恢复期分别为 1.87±0.25，1.92±0.27 μg/L，均明显高于正常对照组 0.37±0.52 ng/L，1.71±0.15 μg/L，差异有显著性(P<0.01)；MPP患儿恢复期血清IL-6含量较急性期明显下降，差异有显著性(P<0.01)，而sIL-6R恢复期与急性期比较差异无显著性(P>0.05)；②非MPP患儿血清IL-6急性期及恢复期分别为1.56±0.26，0.84±0.63 ng/L，明显高于正常对照组，差异有显著性(P<0.01或P<0.05)，而血清sIL-6R与对照组比较差异无显著性(P>0.05)；非MPP患儿急性期血清IL-6高于恢复期，差异有显著性(P<0.05)，血清sIL-6R急性期与恢复期比较差异无显著性(P>0.05)；③MPP患儿急性期血清IL-6、sIL-6R含量较非MPP患儿急性期升高(P<0.01或P<0.05)；MPP患儿恢复期血清IL-6含量与非MPP患儿恢复期的差异无显著性(P>0.05)；MPP患儿恢复期血清sIL-6R含量明显高于非MPP患儿恢复期(P<0.01)。结论：MPP患儿血清IL-6及sIL-6R改变较非MPP患儿明显，提示MPP患儿免疫功能改变较非MPP患儿显著，IL-6及sIL-6R参与了MPP的发生和发展，有必要对MPP患儿进行免疫调节治疗。     

新生儿缺氧缺血性脑病血清白介素-1β和白介素-18测定及意义

目的 探讨新生儿缺氧缺血性脑病（HIE）血清白介素（IL）-1β和IL-18的变化以及二者与HIE临床分度之间的关系。方法采用酶联免疫吸附法（ELISA）检测了70例HIE患儿（按临床分度分轻、中、重三组）及22例正常对照组足月新生儿第三天血清IL-1β和IL-18的水平。结果（1）HIE组新生儿血清IL-1β和IL-18均明显高于对照组（P〈0．05）；（2）与正常对照组比较，中、重度HIE组血清IL-1β和IL-18水平明显增高（P〈0．01）；轻度HIE组血清IL-1β、IL-18水平则与正常对照组无显著性差异（P〉0．05）。HIE组间血清IL-1β及IL-18两两比较，中度与轻度组比较有显著性差异（P〈0．05）；重度组与其他两组比较均明显升高（P〈0．01）。结论急性期HIE患儿血清IL-1β和IL-18水平与HIE临床分度基本一致。因此，血清IL-1β和IL-18水平可作为辅助诊断HIE的指标，对协助HIE临床分度具有重要价值。     

细胞免疫功能在川崎病发病机制中的作用

目的探讨川崎病患儿细胞免疫功能。方法分别采用碱性磷酸酶抗碱性磷酸酶法(APAAP)、ELISA法和双抗体夹心酶联免疫吸附法测定川崎病60例患儿外周血T细胞亚群、血清白细胞介素-2(IL-2)及可溶性白细胞介素-2受体(sIL-2R)水平。结果与对照组比较,川崎病患儿急性期外周血CD3 及CD8 百分率明显下降,CD4 百分率、CD4 /CD8 、血清IL-2及sIL-2R水平明显升高,以上免疫学指标变化在并冠状动脉病变者更为显著。结论川崎病患儿急性期存在细胞免疫功能过度活化及免疫调节功能紊乱。     

肺炎支原体肺炎患儿血清IL—6、IL—2、sIL—2R水平的研究

为对肺炎支原体肺炎(mycoplasma pneamoniae,MP肺炎)免疫学发病机制进一步认识,采用双抗体夹心法对25例MP肺炎患儿急性期血清中IL-2、sIL-2R及IL-6进行检测,结果显示IL-2水平低于对照组(P<0.05);sIL-2R水平明显高于对照组(P<0.01);IL-6高于对照组(P<0.05)。直线相关分析显示,MP肺炎患儿急性期血清IL-6与sIL-2R在感染初期呈正相关(r=0.747),IL-6与IL-2在感染初期无相关性(r=-0.2794)。结果提示细胞因子在MP肺炎发病中起重要作用。     

支气管哮喘患儿诱导痰液中白细胞介素-4及γ-干扰素水平的研究

目的研究支气管哮喘患儿诱导痰液中白细胞介素（IL）-4及γ-干扰素（IFN-γ）水平变化，探讨其在哮喘发病机制中的作用。方法2004年2月～2006年6月儿科住院哮喘患儿36例，用ELISA法测定诱导痰中急性期及缓解期IL-4及IFN-γ水平。结果哮喘患儿诱导痰IL-4水平急性期明显高于缓解期和正常对照组（P〈0．01）；IFN-γ水平急性期低于缓解期及对照组（P〈0．05）；IL-4／IFN-γ比值急性期高于缓解期及对照组（P〈0．05）。急性期患儿诱导痰IL-4水平重症组明显高于轻症组（P〈0．01），IFN-γ水平重症组明显低于轻症组（P〈0．05），IL-4／IFN-γ比值重症组高于轻症组（P〈0．05）。结论哮喘患儿存在Thl／Th2功能紊乱，IL-4及IFN-γ参与哮喘患儿的免疫状态改变，在哮喘发病机制中发挥一定作用。     

哮喘患儿血白细胞介素-2、10、13检测的临床意义

目的　探讨哮喘患儿外周血白细胞介素 2 (IL 2 )、IL 10、IL 13的变化及其在哮喘发病机制中的作用。方法　用ELISA双抗体夹心法测定 16例哮喘患儿及 10例正常儿童血浆IL 2、IL 10、IL 13的含量。结果　哮喘组血浆IL 2、IL 13水平均明显高于正常对照组 ,IL 10水平明显低于正常对照组 (P均 <0 .0 5)。结论　IL 2、IL 10、IL 13等细胞因子参与儿童哮喘发病的病理生理过程 ,可作为病情变化的监测指标     

白细胞介素6及其受体与病毒性心肌炎关系的实验研究

目的　病毒性心肌炎 (VM)目前尚无有效的治疗方法 ,探讨白细胞介素 6 (IL 6 )、可溶性白细胞介素 6受体 (SIL 6R)与病毒性心肌炎的关系 ,并为寻找治疗该病的新方法提供理论依据。方法　通过聚合酶链反应技术选择柯萨奇B病毒性心肌炎患儿 31例作为病例组 ,选择相同例数的同龄健康儿童作为对照组。以酶联免疫吸附试验 (ELISA)法检测实验对象血清中IL 6 ,SIL 6Rα,SIL 6Rβ 水平的变化。所测得的实验数据经统计学处理 ,行 q检验和相关分析。结果　病毒性心肌炎急性期患儿血清中IL 6、SIL 6Rα、SIL 6Rβ 浓度均升高 (P <0 .0 1 ) ;病毒性心肌炎恢复期患儿血清中IL 6、SIL 6Rα、SIL 6Rβ 的水平与正常对照组相比差异无显著性 (P >0 .0 5 ) ;病毒性心肌炎急性期患儿血清中IL 6与SIL 6Rα 浓度变化呈正相关 (r =0 .771 ,P <0 .0 1 ) ,SIL 6Rβ 与IL 6、SIL 6Rα 浓度变化均无相关关系。结论　病毒性心肌炎急性期血清中IL 6水平升高 ,在病毒性心肌炎中发挥炎症防御性作用 ;SIL 6Rα 水平升高 ,且与IL 6水平变化呈正相关 ,是IL 6的激动剂 ,通过扩大IL 6的生物学作用 ,减少心肌细胞的损害。故血清中IL 6、SIL 6Rα 浓度变化可作为VM患者免疫能力监测的指标 ,并预示IL 6、SIL 6Rα 重组分子和激动剂的研制及应用     

Enhanced interleukin-6 and interleukin-8 synthesis in term and preterm infants

There is growing evidence that sepsis-related complications in neonates are crucially mediated by the action of proinflammatory cytokines. It has previously been demonstrated that elevated IL-6 and IL-8 levels can predict brain damage and chronic lung disease in preterm infants. However, it is the current view that neonates have a reduced capability to produce proinflammatory cytokines. To clarify this issue, we analyzed the inflammatory response in term and preterm infants directly at the single cell level by flow cytometry. Endotoxin challenge was performed under defined conditions on monocytes obtained from 50 healthy adults and 119 neonates, which consist of 45 term infants, 63 preterm infants (26.1-36.7 wk of gestational age), and 11 preterm infants with proven infection (24.6-29.9 wk). Our results challenge the existing view of an immature inflammatory response by demonstrating that term infants and preterm infants display a higher percentage of IL-6- and IL-8-positive cells than adults. After preincubation with dexamethasone the number of cytokine-positive cells decreased in all groups, but the number of IL-8-positive cells remained higher in term and preterm infants >32 wk compared with adults. These observations demonstrate not only a well-developed but also an enhanced inflammatory response in term and preterm infants. Under consideration of several detrimental effects of IL-6 and IL-8, our data may have major implications on the pathophysiology of inflammatory-triggered neonatal diseases.     

Serum interleukin-1 alpha and soluble interleukin-2 receptor concentrations in cystic fibrosis

Interleukin (IL)-1 and IL-2 may participate in the systemic inflammatory response and hypergammaglobulinaemia observed in patients with cystic fibrosis. Thirty seven patients with cystic fibrosis were compared with 25 normal controls. High IgG and IgM concentrations were associated with more severe pulmonary disease. IL-1 alpha and soluble IL-2 receptor concentrations were higher in the cystic fibrosis group than in the controls and also correlated with concentrations of IgG and IgM. These results suggest that these cytokines may contribute to enhanced immunoglobulin synthesis and silent inflammatory activity in clinically stable patients with cystic fibrosis.     

Plasma levels of interleukin-6 and interleukin-10 in preterm neonates evaluated for sepsis

In a prospective study, plasma interleukin-6 (IL-6) and interleukin-10 (IL-10) levels were measured by enzyme-linked immunosorbent assay in 45 premature neonates (25–34 weeks gestational age) with signs and symptoms of suspected sepsis at 0, 12 and 24 h; C-reactive protein (CRP) was measured at 0–24 h after enrolment. Six subjects were excluded due to insufficient blood sampling. The remaining 39 neonates were assigned to one of three groups: 25 newborns with sepsis (blood culture positive), seven with pneumonia (positive results on broncho-alveolar lavage fluid culture and characteristic chest radiography) and seven with necrotising enterocolitis (NEC) (characteristic intestinal and radiological signs according to the criteria of Bell et al.). A group of 20 healthy preterm neonates represented control subjects. On admission, higher levels of IL-6, IL-10 and CRP were observed in neonates with sepsis: IL-6 (median 1500 pg/ml, range 487–10000 pg/ml), IL-10 (median 113 pg/ml, range 70–196 pg/ml), CRP (median 22 mg/l, range 4–80 mg/l); pneumonia: IL-6 (median 1500 pg/ml, range 747–8000 pg/ml, IL-10 (median 84 pg/ml, range 76–92 pg/ml), CRP (median 10 mg/l, range 8–33 mg/l) and NEC: IL-6 (median 6650 pg/ml, range 1595–7950 pg/ml), IL-10 (median 80 pg/ml, range 61–147 pg/ml), CRP (median 3 mg/l, range 2.8–8 mg/l) as compared to controls (IL-6 median 208 pg/ml, range 198–349 pg/ml; IL-10 median 36 pg/ml, range 19–50 pg/ml; CRP median <2 mg/l) (P < 0.05). In neonates with sepsis, IL-6 levels were significantly correlated with IL-10 levels (r=0.65; P=0.04) at the time of the second sample. The highest IL-6 levels were observed at onset, while IL-10 was predominant 12 h later. On admission, IL-10 and CRP levels were significantly higher in non-survivors (IL-10 median 507 pg/ml, range 422–753 pg/ml; CRP median 123 mg/l, range 20–219 mg/l) than in survivors (IL-10 median 76 pg/ml, range 61–143 pg/ml; CRP median 8 mg/l range 3–46 mg/l), while IL-10 levels were significantly higher (P < 0.05) also 12 h after admission (non-survivors: IL-10 median 600 pg/ml, range 538–800 pg/ml; survivors: IL-10 median 74 pg/ml, range 53–161 pg/ml). IL-6 and IL-10 levels were significantly correlated with CRP levels on admission (r=0.45; P=0.05). Conclusion Preterm neonates with sepsis, pneumonia or necrotising enterocolitis showed increased interleukin-6, interleukin-10 and C-reactive protein levels. High interleukin-10 concentration was associated with mortality and could be an early indicator of prognosis. Received: 21 November 2000 / Accepted: 23 January 2001     

Serum interleukin-1 alpha and soluble interleukin-2 receptor concentrations in cystic fibrosis.

Interleukin (IL)-1 and IL-2 may participate in the systemic inflammatory response and hypergammaglobulinaemia observed in patients with cystic fibrosis. Thirty seven patients with cystic fibrosis were compared with 25 normal controls. High IgG and IgM concentrations were associated with more severe pulmonary disease. IL-1 alpha and soluble IL-2 receptor concentrations were higher in the cystic fibrosis group than in the controls and also correlated with concentrations of IgG and IgM. These results suggest that these cytokines may contribute to enhanced immunoglobulin synthesis and silent inflammatory activity in clinically stable patients with cystic fibrosis.     

Plasmatic levels of interleukin-1beta and interleukin-6 in newborn infants with fever

OBJECTIVE: To study plasma levels of IL-1beta and IL-6 in order to distinguish the presence of bacterial infection in newborn infants with fever. METHODS: A cohort of 117 newborn infants with postnatal age equal to or less than 5 days, with no previous use of antibiotic therapy, and with clinical suspicion of bacterial infection was studied from July 1995 through August 1996. Those with definite criteria for sepsis were considered infected. Fever was defined as axillar temperature > 37.5 degrees C in three independent measurements. The patients were classified in four different groups: Group 1: infected with fever; Group 2: infected without fever; Group 3: not infected with fever; Group 4: not infected without fever. Complete blood count, platelet count, blood or other fluid cultures, and plasmatic levels of IL-1beta and IL-6 were collected before the beginning of antibiotic therapy. RESULTS: Of the 117 newborn infants studied were 66 infected and 51 not infected. Fever was present in 45 (38.46%). The median values of IL-1beta and IL-6 were significantly higher in newborn infants with fever than in those with no fever. There were significant differences between groups 1 and 2, 1 and 4, and 2 and 3 for IL-1beta. There were no significant differences between groups 2 and 4, and 1 and 3 for IL-1beta. Eight (72%) newborn infants with no infection and no fever had environment heating, and 3 had dehydration. There were no differences in median IL-6 levels between groups 1 and 2, and 3 and 4. There were significant differences in the median IL-6 levels between groups 1 and 3, and 1 and 4. CONCLUSIONS: IL- 6 is a marker of early neonatal sepsis. IL-1beta is related to neonatal fever response independently of the presence of bacterial infection.