血清热休克蛋白70、白细胞介素-4和白细胞介素-17在过敏性紫癜中的临床意义

目的 探讨血清热休克蛋白70(HSP70)、白细胞介素(IL)-4和IL-17水平检测在过敏性紫癜(HSP)中的临床意义,同时了解其对HSP患儿的诊断价值。方法 选取2020年9月至2022年4月在该院初次就诊的158例HSP患儿作为观察组,另选取同期50例健康体检儿童作为健康对照组。分别收集观察组(急性期和恢复期)、健康对照组的血液标本,采用酶联免疫吸附试验检测并比较两组儿童HSP70、IL-4及IL-17的水平变化情况;采用Spearman相关分析HSP70水平与IL-4、IL-17水平的相关性;采用受试者工作特征曲线(ROC曲线)分析血清HSP70、IL-4和IL-17水平对HSP的临床诊断效能。结果 与健康对照组比较,观察组血清HSP70、IL-4和IL-17水平均明显升高,差异均有统计学意义(P<0.05);急性期HSP患儿HSP70、IL-4、IL-17水平均明显高于恢复期,差异均有统计学意义(P<0.05)。Spearman相关分析结果显示,急性期HSP患儿HSP70水平与IL-4、IL-17水平均呈明显正相关(r=0.784、0.553,P<0.001...     

小儿毛细支气管炎血白细胞介素-6及-18检测结果分析

目的:研究白细胞介素(IL)-6及IL-18在急性毛细支气管炎(毛支)患儿血清中的水平及检测价值。方法:对58例小儿毛支(观察组)急性期采用酶联免疫吸附法检测血IL-6、IL-18水平,选择同期门诊体检的健康儿童17例作为正常对照组。将观察组根据病情程度分为轻、中、重3组,比较不同病情毛支患儿的IL-6、IL-18水平。结果:观察组IL-6水平(24.4±126.2)ng/L,对照组(81.3±188.1)ng/L,两组比较无显著差异(P>0.05);观察组IL-18水平(344.7±365.1)ng/L,显著高于对照组的(98.7±91.2)ng/L(P<0.05);观察组轻、中、重度3组之间IL-6、IL-18水平差异均无统计学意义。结论:小儿毛支急性期血清IL-18升高,IL-6无明显变化,提示Th1型细胞因子的免疫反应在本病发病中起重要作用。     

少儿毛细支气管炎血白细胞介素-6及-18检测结果分析

目的:研究白细胞介素(IL)-6及IL-18在急性毛细支气管炎(毛支)患儿血清中的水平及检测价值.方法:对58例小儿毛支(观察组)急性期采用酶联免疫吸附法检测血IL-6、IL-18水平,选择同期门诊体检的健康儿童17例作为正常对照组.将观察组根据病情程度分为轻、中、重3组,比较不同病情毛支患儿的IL-6、IL-18水平.结果:观察组IL-6水平(24.4±126.2)ng/L.对照组(81.3±188.1)ng/L,两组比较无显著差异(P＞0.05);观察组IL-18水平(344.7±365.1)ng/L,显著高于对照组的(98.7±91.2)ng/L(P＜0.05);观察组轻、中、重度3组之间IL-6、IL-18水平差异均无统计学意义.结论:小儿毛支急性期血清IL-18升高,IL-6无明显变化,提示Th1型细胞因子的免疫反应在本病发病中起重要作用.     

白细胞介素-29与Toll样受体4在过敏性紫癜患儿中的表达及临床意义

目的观察白细胞介素(IL)-29、Toll样受体(TLR)4在过敏性紫癜(HSP)患儿中的表达及临床意义。方法选择48例HSP患儿作为观察组,20例健康儿童作为对照组,实时荧光定量PCR检测对照组和观察组(急性期、恢复期)外周血单个核细胞(PBMC)中IL-29mRNA、TLR4mRNA的表达水平,并检测不同时期血清中IL-29、TLR4、IL-4、免疫球蛋白(Ig)A、IgM、IgG、C3、C4、β~2微球蛋白(β~2-MG)水平。结果观察组急性期PBMC中IL-29、TLR4mRNA相对表达水平,以及血清中IL-29、TLR4水平明显高于恢复期和对照组,差异均有统计学意义(P0.05)。观察组急性期IgA、C3、IL-4、β~2-MG水平明显高于对照组,差异均有统计学意义(P0.05)。血清中IL-29与TLR4呈显著正相关(P0.05);血清中IL-29与IgA、C3、IL-4、β~2-MG呈显著正相关(P0.05);血清中TLR4与IgA、C3、IL-4、β~2-MG呈显著正相关(P0.05)。结论 IL-29、TLR4参与了HSP的发生、发展,维持了机体的炎症水平。     

肺炎支原体肺炎患儿血清中白细胞介素水平与伴发喘息的相关性

目的研究和分析肺炎支原体肺炎(MPP)患儿血清中白细胞介素水平与伴发喘息的相关性。方法选取136例MPP患儿作为病例组,根据是否伴发喘息将其分为喘息组59例和非喘息组77例,根据病情将喘息组分为急性期组26例和缓解期组33例,选取60例健康儿童作为对照组。对各组患儿及对照组儿童的血清白细胞介素-4(IL-4)、白细胞介素-5(IL-5)、白细胞介素-13(IL-13)水平进行测定和比较。结果喘息组、非喘息组、对照组儿童血清IL-4、IL-5、IL-13水平的差异均有统计学意义(F=16.332、112.369、96.411,P0.05);急性期组、缓解期组、对照组儿童血清IL-4、IL-5、IL-13水平的差异均有统计学意义(F=24.058、174.212、143.720,P0.05);病例组患儿的血清IL-4水平与IL-5水平呈正相关关系(P0.05),而IL-4水平与IL-13水平、IL-5水平与IL-13水平均无相关性(P0.05)。结论 MPP患儿表现为IL-4、IL-5、IL-13等血清白细胞介素水平的升高。     

血清白细胞介素-6和白细胞介素-8在重症急性胰腺炎早期诊断中的意义

目的 探讨血清白细胞介素-6(IL-6)、白细胞介素-8(IL-8)等细胞因子在早期诊断重症急性胰腺炎(SAP)中的价值.方法 以Ranson和APACHE-Ⅱ评分为标准,把36例急性胰腺炎患者分成轻症胰腺炎组(MAP)及重症胰腺炎组(SAP),选择年龄匹配的13名健康志愿者为对照组.在患者入院24 h内采静脉血并检测血清中IL-6、IL-8水平.结果 二种细胞因子血清水平均为SAP组最高,对照组最低,其中IL-6水平在3组之间、两两比较差异均有统计学意义(均P<0.05),IL-8水平在对照组与SAP组之间、MAP组与SAP组之间差异有统计学意义(均P<0.05),而对照组与MAP组比较差异无统计学意义(P>0.05).结论 IL-6、IL-8对早期鉴别诊断轻症胰腺炎和重症胰腺炎均有重要的临床意义.     

肺炎支原体肺炎患儿血清中白细胞介素水平与伴发喘息的相关研究

目的探讨肺炎支原体肺炎患儿血清中白细胞介素4(IL-4)、白细胞介素5(IL-5)、白细胞介素13(IL-13)水平及其与喘息发生的关系。方法收集2013年1~10月123例肺炎支原体肺炎患儿,根据临床表现分为喘息组53例和无喘息组70例,喘息组根据临床病情分为急性期喘息组23例和缓解期喘息组30例,同时收集同期50例无喘息健康儿童血清作对照,采用酶联免疫吸附试验(ELISA)测定血清中IL-4、IL-5、IL-13水平。结果肺炎支原体肺炎患儿血清中IL-4、IL-5、IL-13水平高于健康对照组,喘息组患儿血清中IL-4、IL-5、IL-13水平高于无喘息组患儿,血清IL-4、IL-5、IL-13在急性期喘息组、缓解期喘息组中水平差异具有统计学意义(P0.05)。患儿血清中IL-4、IL-5水平呈正相关(r=0.613,P0.05),其余指标无相关性。结论血清IL-4、IL-5、IL-13在肺炎支原体肺炎伴喘息患儿中水平升高,且伴随着喘息症状的加重水平上升,对肺炎支原体肺炎的治疗有指导意义。     

毛细支气管炎患儿细胞因子及EOS水平变化分析

目的：通过对毛细支气管炎（毛支）患儿及支气管肺炎非喘息型患儿（肺炎）血清中白细胞介素Interleu-kin2、6、8（IL-2、6、8）和外周血嗜酸性粒细胞（EOS）水平的检测,探讨细胞因子在毛支发病中所起的作用。方法：符合毛支诊断标准的患儿60例,对照组支气管肺炎患儿60例。空腹静脉取血,用放射免疫法测定血清IL-2、6、8水平,测外周血EOS计数。结果：毛支组血清IL-6、8较肺炎组显著增高,差异有统计学意义（P〈0.05）,外周血EOS计数差异无统计学意义（P〉0.05）。结论：毛支发生、发展过程中,由于各种感染因素刺激气道导致细胞因子水平增高,参与抵御病原体侵犯的同时,也造成局部肺组织的不同损伤。提示在治疗毛支时除以清除病毒为主外还应注意抑制炎症递质的产生和免疫功能的调节。     

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.     

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。     

白细胞介素-17与白细胞介素-35在自身免疫性疾病中的研究进展

自身免疫性疾病是免疫耐受性破坏的结果,最终导致组织损伤,但病因尚未阐明。辅助性T细胞(Th17)、调节性T细胞(Treg)、Treg/Th17失衡及其相关细胞因子与自身免疫性疾病的发生发展密切相关。白细胞介素(IL)-17主要由Th17分泌,具有促炎效应,参与各种自身免疫性疾病发生发展。IL-35是IL-12家族的一种新型细胞因子,主要由Treg产生,具有免疫负性调节作用,是Th17/Treg相关的重要细胞因子。本文就IL-17与IL-35的功能、效应机制及其在自身免疫性疾病中的作用等进行综述,以为该病的治疗提供理论基础。     

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.     

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     

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.     

Colony promoting activity: differences from interleukin-3 and similarities to interleukin-6

The supernatant of long-term bone marrow culture contains colony promoting activity (CPA) which does not have granulocyte-macrophage colony stimulating activity (CSF) but which enhances granulocyte-macrophage (GM) colony formation in the presence of CSF. CPA might consist of IL-3 or IL-3-like activity, since CPA stimulates proliferation and differentiation of more immature cells to CSF-responding granulocytes-macrophage progenitors (GM-CFC), and since IL-3 also stimulates immature hemopoietic cells to proliferate and differentiate to functional blood cells. IL-1 and IL-6 are also known to enhance GM colony formation. One or both of these molecules can accordingly be another candidate for CPA. In the present study, GM-CSF activity of IL-3 was dependent on the batch of serum: it was negative in the presence of fetal calf serum, but positive in the presence of horse serum. In contrast, GM-CSF and CPA showed no such dependence on the batch of serum. The addition of IL-3 to GM colony assay system did not enhance but rather suppressed GM colony formation. The supernatant of long-term bone marrow culture which contains substantial levels of CPA did not stimulate proliferation of IL-3 dependent DA-1 cells, but facilitated the proliferation of IL-6 dependent, MH60.BSF2 cells. No detectable level of IL-1 activity was found in the supernatant. These results indicate that CPA is different from IL-1, IL-3 or GM-CSF, but similar to or the same as IL-6.     

白细胞介素-18和白细胞介素-12在儿童1型糖尿病酮症酸中毒中的作用

目的探讨白细胞介素-18(IL-18)、白细胞介素-12(IL-12)和干扰素-γ(INF-γ)在儿童1型糖尿病酮症酸中毒(DKA)中的作用。方法采用酶联免疫吸附(ELISA)方法检测61例儿童1型糖尿病(T1DM)患儿(其中28例伴DKA,33例无DKA)和30例正常对照者IL-18、IFN-γ和IL-12的血清水平。结果(1)T1DM患儿中血清IL-18水平明显比对照组高[(691．99±381．42) pg/ml vs(310．02±265．32)pg/ml,P=0．03],而两组间IFN-γ和IL-12水平则无差别。(2)DKA组患儿中IL-18和IFN-γ血清水平明显高于无DKA组[(759．25±353．82)pg/ml vs(634．93±399．79)pg/ ml,P=0．001和(9．35±8．06)pg/ml vs(5．21±6．47)pg/ml,P=0．044],而两组间IL-12血清水平则无差别。(3)IL-18和IFN-γ呈相关趋势,而与IL-12正相关。结论DKA患儿IL-18和IFN-γ血清水平明显升高,提示其可能在DKA的发生、发展中起重要作用。