miRNA-21在支气管哮喘发生发展中的研究进展

支气管哮喘是一种以慢性气道炎症和气道高反应性为特征的异质性疾病。微小核糖核酸（miRNA）是小的非编码核糖核酸,通常由18～25个核苷酸组成,在多种呼吸系统疾病中发挥作用。miRNA-21是微小核糖核酸家族的重要成员,在支气管哮喘的发生发展中发挥重要作用。笔者对miRNA-21在支气管哮喘气道炎症、气道高反应性、气道重塑中的作用,miRNA-21的相关靶点以及其在支气管哮喘中的临床价值进行综述。     

miRNA-26a 在良、恶性腹水鉴别诊断中的意义

目的：探讨miRNA-26a在良、恶性腹水鉴别诊断中的意义。方法收集北京大学深圳医院2011年9月~2014年3月门诊及住院患者60例,包括20例肝硬化腹水患者（肝硬化腹水组）,20例结核性腹水患者（结核性腹水组）,20例恶性腹水患者（恶性腹水组）。采用实时定量PCR（qRT-PCR）方法检测并比较各组血清miRNA-26a、甲胎蛋白（AFP）、糖类抗原125（CA125）的表达。结果恶性腹水组血清CA125表达高于结核性腹水组和肝硬化腹水组,但差异无统计学意义（P〉0.05）。 AFP、miRNA-26a在结核性腹水组及肝硬化腹水组表达差异无统计学意义（P〉0.05）;AFP和miRNA-26a在恶性腹水组患者血清表达明显高于结核性腹水组和肝硬化腹水组,差异有统计学意义（P〈0.05）。结论 miRNA-26a水平将来有可能有助于良、恶性腹水的鉴别诊断。     

宫颈癌组织中miRNA-21、miRNA-127和miRNA-125a的表达变化及临床指导意义

目的评估宫颈癌组织中miRNA-21、miRNA-127和miRNA-125a的表达变化及临床指导意义。方法对2014年1月至2017年12月期间在三峡大学宜昌市第二人民医院治疗的95例宫颈癌临床资料进行回顾性分析,统计宫颈癌组织及癌旁组织中miRNA-21、miRNA-127和miRNA-125a表达量,并分析miRNA-21、miRNA-127和miRNA-125a表达与宫颈癌患者临床病理学特征之间的关系,同时分析宫颈癌组织中miRNA-21、miRNA-127和miRNA-125a表达与患者生存的关系。结果宫颈癌组织中miRNA-21表达量(25.63±6.85)明显高于癌旁组织(1.33±0.62)(P <0.001)。宫颈癌组织中miRNA-127 (5.64±1.29)和miRNA-125a (8.47±1.58)表达量明显低于癌旁组织中miRNA-127 (16.47±4.62)和miRNA-125a (23.49±5.57)表达量(P <0.001)。宫颈癌组织中的miRNA-21、miRNA-127和miRNA-125a表达与宫颈肌层浸润、组织学分化、淋巴... 更多     

CHL1在支气管哮喘中的表达及意义

目的：探讨神经细胞黏附分子L1样蛋白（cell adhesion molecule L1?like protein,CHL1）在支气管哮喘中的表达及潜在机制。方法：收集55例哮喘患者及同期18例健康对照的临床资料及血清标本,酶联免疫吸附法检测血清CHL1水平,分析其与肺功能指标、血清总免疫球蛋白E（immunoglobulin E,IgE）的相关性。构建卵清蛋白（ovalbumin,OVA）诱导的慢性过敏性哮喘小鼠模型,免疫组化观察小鼠肺组织CHL1的表达定位及分布。采用不同细胞因子刺激人支气管上皮细胞（16HBE）,分别用实时定量PCR法和蛋白质免疫印迹法检测细胞CHL1 mRNA和蛋白表达情况。结果：与对照组（4.174±2.122）ng/mL相比,哮喘患者血清CHL1水平明显增高［（7.497±3.274）ng/mL,P < 0.000 1］,与血清总IgE水平呈正相关（r=0.287,P=0.048）。CHL1主要表达于小鼠肺组织支气管上皮细胞,哮喘小鼠表达量较对照组升高。TGF?β可上调支气管上皮细胞CHL1 mRNA及蛋白表达水平。结论：哮喘中支气管上皮细胞CHL1表达增加,该过程可能与TGF?β相关信号通路有关。     

miRNA-126和miRNA-92 a在冠心病患者血清中的表达水平及临床意义

目的:探究miRNA-126和miRNA-92a在冠心病(CHD)患者血清中表达水平及临床价值.方法:选择56例CHD患者和30例健康体检者为对象.测定两组血清脂代谢指标、细胞因子、miRNA-126和miRNA-92a含量,Gensini评分法评估两组冠脉病变程度.ROC分析血清miRNA-126和miRNA-92a...     

CD25及FOXP3在支气管哮喘小鼠中的表达以及地塞米松的干预作用

目的 分析哮喘小鼠模型肺组织及骨髓中CD25及FOXP3的表达,以及地塞米松的干预作用.方法 BALB/c小鼠随机分为正常对照、哮喘及地塞米松干预组,通过HE染色观察肺组织的病理变化,应用Western blot、RT-PCR方法检测肺组织FOXP3及CD25的表达,RT-PCR方法检测哮喘及地塞米松干预组肺及骨髓FOXP3 mRNA表达.结果 哮喘及地塞米松干预组肺组织FOXP3表达强于正常对照组(P<0.05),地塞米松干预促进FOXP3表达(P<0.05);哮喘及地塞米松干预组肺组织CD25表达强于正常对照组(P<0.05),而两组之间无明显差异(P>0.05);哮喘及地塞米松干预组肺组织及骨髓细胞均有FOXP3 mRNA表达,且地塞米松组强于哮喘组(P<0.05).结论 哮喘小鼠肺内CD25及FOXP3表达增强,地塞米松会促进其表达;哮喘小鼠骨髓有F10XP3表达,地塞米松促进其表达.     

激活蛋白-1在哮喘患儿支气管上皮细胞的表达

近年的研究发现 ,哮喘与支气管上皮细胞表达多种炎性蛋白有关[1] ,但导致炎性蛋白合成的机制不明。激活蛋白 1(ａｃｔｉｖａｔｏｒｐｒｏｔｅｉｎ 1,ＡＰ 1)是一种转录因子 ,体外研究发现 ,活化后的ＡＰ 1可调控上述炎性蛋白的合成 ,因此推测在哮喘患者体内 ,导致炎性蛋白合成的原因可能与ＡＰ 1活化有关。我们试图通过观察ＡＰ 1的两个组成亚单位ｃ ｆｏｓ和ｃ ｊｕｎ在哮喘患儿支气管上皮细胞的表达 ,了解ＡＰ 1是否活化 ,探讨其在哮喘中的作用。一、对象与方法1 对象 :(1)哮喘组 :选取 1998年 1月至 1998年 10月在北京市儿童医院住院的哮…     

ox-LDL对巨噬细胞表达miRNA-155和miRNA-146a／b的影响

目的：探讨氧化低密度脂蛋白（ox—LDL）刺激对巨噬细胞表达miRNA-155和miRNA-146a／b的影响。方法：培养人巨噬细胞,随机分为三组：空白对照组、ox-LDL（10μg／mL）组和OX—LDL（20μg／mL）组,刺激6h后,收集细胞,实时定量PCR方法检测miRNA-155和miRNA—146a／b的表达。结果：OX—LDL刺激可以增加巨噬细胞表达miRNA-155和miRNA-146a／b,且呈浓度依赖性。结论：miRNA-155和miRNA-146a／b可能参与ox-LDL致动脉粥样硬化过程。     

miR-26a对小鼠骨髓间充质干细胞成骨分化能力的调控作用

 目的 利用小鼠骨髓间充质干细胞（BMSCs）的成骨分化模型, 探讨 miR-26a 在成骨分化中的表达趋势及调控作用。方法 提取雌性C57/BL6J小鼠双侧下肢股骨骨髓分离培养BMSCs,诱导分化为成骨细胞,通过实时定量PCR检测miR-26a在BMSCs及其诱导分化细胞中的表达。使用miR-26a的促进物miR-RiboTM microRNA-26a mimics通过siPORTTMNeoFXTMagent转染试剂瞬时转染BMSCs并加入成骨诱导剂培养,并同时设立转染microRNA-26a mimics NC的对照组。培养7 d、14 d后,进行细胞形态、碱性磷酸酶（ALP）染色、钙盐结节（茜素红染色）等项目的检测。另外制造绝经后骨质疏松小鼠模型（OVX组）与假手术动物模型（sham组）,RT-PCR检测OVX组中miR-26a的表达。结果 miR-26a的表达在BMSCs向成骨分化过程中上升约25倍,成骨基因表达也随着诱导时间的增加逐渐升高。转染miR-26a mimics后的BMSCs在培养7d后逐渐由梭形变为多角形,与阴性对照组类似;ALP染色显示阴性对照组培养7 d后为阳性,而实验组在培养7 d时呈强阳性;茜素红染色显示实验组培养14 d后出现数量较多的钙盐沉积结节,而阴性对照组则较少。miR-26a mimics组成骨基因的表达均高于对照组。RT-PCR检测结果显示OVX组中miR-26a的表达低于sham组4倍。结论 miR-26a mimics的转染可以促进BMSCs的成骨分化潜能,在骨质疏松的环境中miR-26a表达下降,间接证实了miR-26a对小鼠BMSCs成骨潜能的促进作用。     

ADAM15在支气管哮喘表达及意义

目的:研究整合素金属蛋白酶15(a disintegrin and metalloproteinase 15,ADAM15)在支气管哮喘中表达及可能机制.方法:收集本院32例哮喘患者及同期16例健康对照的临床资料及血清标本,酶联免疫吸附法检测血清ADAM15水平,分析其与外周血嗜酸性粒细胞数、血清总IgE相关性.构建O...     

Inhibition of allergic responsiveness in a murine asthma model via IFN-γ transgene expression

Objective To investigate adenoviral vector mediated exogenous gene expression in mouse lungs and the effect of mIFN-γ transgene expression on allergen-induced pulmonary eosinophil infiltration in a murine asthmatic model. Methods LacZ marker gene was transduced into CD-1 mouse airway epithelial cells by installation of a replication-deficient adenovirus with LacZ gene (AdCMVLacZ) 5×10[9]plaque forming unit (pfu) in the intratrachea or nostril.C57 mice were sensitized intraperitoneally and challenged by aerosol with ovalbumin (OVA) to produce an asthmatic model.AdCMVmIFNγ 5×10[9] pfu was administered via nostril in asthmatic mice 48 h before OVA challenge.Sera, bronchial alveolar lavage (BAL) and lungs were recovered 48 h after OVA challenge.Results After administration with AdCMVLacZ by intratracheal installation or nose-drop, the lungs revealed a high level of widespread LacZ transduction with X-gal staining, mainly along airways.IFN-γ via adenoviral vector transduction could be overexpressed both in vitro and in vivo (1624.7±1321.5 pg/ml in BAL 96 h after AdCMVIFNγ infection).In AdCMVIFNγ treated asthmatic models, histological evaluation revealed marked suppression of eosinophil peribronchial and perivascular infiltration; the recoverable percentage of eosinophils in BAL was an average of 9.00%±4.58%, which was a statistically significant decrease versus that of the positive control group (75.13%±6.85%) (P&lt;0.001).The total cell number in BAL ((145±55.6)×10[3 cells/ml) in AdCMVmIFNγ treated mice also was tremendously reduced compared to the positive control group ((216.6±71.1)×10[3 ]cells/ml).Conclusions Adenoviral vector was able to overexpress exogenous gene in murine lungs.IFN-γ overexpression via adenoviral vector in pulmonary epithelia in vivo can abrogate allergen-induced eosinophilic infiltration in lungs in an asthmatic model, which may suggest a new preventively therapeutic method for cytokine immunogenetic transfer in allergic asthma.     

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.

     

CD69 expression on airway eosinophils and airway inflammation in a murine model of asthma

Background Asthma is a chronic airway disease with inflammation characterized by physiological changes （airway hyper-responsiveness, AHR） and pathological changes （inflammatory cells infiltration and mucus production）. Eosinophils play a key role in the allergic inflammation. But the causative relationship between eosinophils and airway inflammation is hard to prove. One of the reasons is lack of activation marker of murine eosinophils. We investigated the expression of CD69 on murine eosinophils in vitro, the relationship between the expression of CD69 on eosinophils from peripheral blood and bronchoalveolar lavage fluid and on airway inflammation in asthmatic mice. Methods Eosinophils from peripheral blood of IL-5 transgenic mice （NJ.1638） were purified. Mice were divided into five groups： wild type mice sensitized and challenged with saline （WS group）, wild type mice sensitized and challenged with ovalbumin （WO group）, IL-5^-/- mice sensitized and challenged with saline and transferred with purified eosinophils （ISE group）, IL-5^-/- mice sensitized and challenged with OVA and transferred with purified eosinophils （IOE group）, IL-5^-/- mice sensitized and challenged with OVA and transferred with purified eosinophils, pretreated with anti CD4 monoclonal antibody （IOE＋antiCD4mAb group）. IL-5^-/- mice were sensitized with OVA at day 0 and day 14, then challenged with OVA aerosol. On days 24, 25, 26 and 27 purified eosinophils were transferred intratracheally to IL-5^-/- mice. On day 28, blood and BALF were collected and CD69 expression on eosinophils measured by flowcytometry. Results Purified eosinophils did not express CD69. But eosinophils cultured with PMA＋MA, IFN- T, IL-5 or GM-CSF expressed CD69 strongly. Eosinophils from blood of WO, WS group did not express CD69 at all. The numbers of eosinophils in BALF of WO group, IOE group, ISE group and IOE＋antiCD4mAb group were significantly higher than in mice of WS group which did not have eosinophils at all. CD69 expression on eosinophils in BALF of IOE and WO groups was strong. Eosinophils in BALF of ISE and IOE＋antiCDmAb groups did not express CD69. The mucus production result was similar to CD69 expression. There were eosinophils infiltration in lung slides of all groups except WS group. Conclusion Activation in airway of eosinophils could directly lead to airway inflammation.     

Active immunotherapy of allergic asthma with a recombinant human interleukin-5 protein as vaccine in a murine model

Background Eosinophils are highly related to allergic asthma inflammation. Interleukin (IL)-5 is the major chemokine of eosinophils, inhibition of the activity of IL-5 thus seems to be a potential approach to asthma therapy. The current study was performed to determine whether a recombinant human IL-5 protein as a xenogeneic vaccine has the capability of inducing anti-asthma activities.Methods Recombinant human IL-5 was used as a protein vaccine. Mouse asthma model was established to observe the anti-asthma activities. Lung histology was observed; eosinophils in blood and bronchoalveolar lavage were stained and counted. Airway hyperresponsiveness was determined by whole body plethysmograph. Antibody characters and cytokines were detected with enzyme linked immunosorbent assay (ELISA) and Western blot assay.Results Vaccination with recombinant human IL-5 protein as vaccine significantly reduced airway inflammation and airway hyperresponsiveness, and shifted the cytokine production from Th2 (IL-4) to Th1 (INF-γ) in mice allergic-asthma model. Immunization with recombinant human IL-5 protein vaccine bypassed the immunological tolerance and induced production of polyclonal antibodies that were cross-reactive with murine IL-5.Conclusions Active immunization with xenogeneic homologous IL-5 may be a possible therapeutic approach to the treatment of asthma and potentially of other eosinophilic disorders.     

miRNA-7在小鼠不同组织器官中表达的检测及其意义

目的 采用Real-time PCR方法来检测miRNA-7在小鼠12种不同组织器官中的表达情况并探讨其意义.方法 首先分别提取小鼠12种组织器官总RNA,用miRNA-7特异性引物逆转录为cDNA,采用Real-time PCR探针法检测miRNA-7在12种组织器官中的表达水平.结果 成功应用Real-time PCR方法检测miRNA-7在小鼠12种组织器官中的表达水平,结果显示,miRNA-7在肺组织中的表达水平最高,而在淋巴结中的表达水平最低.此外,在小肠、脑、胸腺、脾脏中也存在miRNA-7的高表达.结论 miRNA-7在小鼠的肺、小肠、脑、胸腺、脾脏中呈较高水平的表达,提示该分子可能在上述器官的发育、分化、功能维持及相关疾病发生中具有重要作用,为后续深入研究miRNA-7的生物学功能提供了前期试验依据.     

IL-12真核表达质粒对小鼠气道变应性炎症的免疫调节作用

目的:研究IL-12真核表达质粒(psIL-12)在气道内表达对成年小鼠气道变态反应炎症的影响.方法:以卵白蛋白(OVA)复制成年小鼠气道变态反应炎症模型,气道内应用单剂量psIL-12,pcDNA3.1(+),PBS/脂质体复合物,同时设正常对照组.分别检测肺单链IL-12表达,计数支气管肺泡灌注液(BALF)中嗜酸粒细胞的百分比和IL-4,IFN-γ含量,观察肺组织形态学变化.结果:气道转染psIL-12可在小鼠肺组织中表达IL-12mRNA;psIL-12干预组BALF中嗜酸粒细胞百分比为(2.6±2.3)%,较PBS对照组(11.6±2.3)%明显降低,两组组间差异具有显著性(P<0.05).psIL-12干预组BALF中IL-4含量为(103±53)ng/L,IFN-γ含量为(171±20)ng/L,而PBS对照组IL-4含量为(319±12)ng/L,IFN-γ含量为(77±36)ng/L,两组组间差异具有统计学意义(P<0.05).psIL-12可明显阻止模型鼠肺组织病理改变,降低血清中OVA特异性IgE抗体含量.结论:psIL-12转染气道表达IL-12,增加Th1型细胞因子IFN-γ的产生,...     

哮喘易感基因ORMDL3在哮喘小鼠中的表达及地塞米松的干预作用

目的:探讨哮喘易感基因ORMDL3在支气管哮喘发病时的表达及地塞米松的干预作用?方法:将30只健康清洁级雌性Balb/c小鼠随机分为3组:对照组?哮喘组(卵蛋白致敏)?地塞米松组(卵蛋白致敏,激发前腹腔注射地塞米松1 mg/kg进行干预),每组10只?称量和观察小鼠的体重增长趋势,对小鼠肺组织进行HE染色评价浸润情况,计数3组小鼠的外周血嗜酸性粒细胞,ELISA法检测对比3组小鼠血清白介素4(IL-4)的浓度变化,采用反转录-聚合酶链反应(RT-PCR)方法检测小鼠肺组织ORMDL3 mRNA水平表达?结果:哮喘组小鼠体重增长显著落后于其他两组(P < 0.05),地塞米松干预后能缓解生长迟滞,但仍低于对照组(P < 0.05)?病理组织学显示哮喘组小鼠肺组织见大量嗜酸性粒细胞浸润,黏膜下层和平滑肌增厚,管腔狭窄,地塞米松组小鼠肺组织改变较哮喘组为轻?哮喘组外周血嗜酸性粒细胞计数显著高于对照组和地塞米松组(P < 0.05),地塞米松组计数高于对照组(P < 0.05)?哮喘组小鼠的IL-4水平显著高于对照组(P < 0.05),经地塞米松干预后IL-4水平显著降低(P < 0.05),但仍高于对照组?哮喘组小鼠ORMDL3 mRNA的表达水平较对照组显著升高,地塞米松组小鼠ORMDL3 mRNA水平较哮喘组下降,但未达统计学意义(P > 0.05)?结论:卵清蛋白小鼠哮喘模型中ORMDL3的mRNA表达显著增高,地塞米松可下调ORMDL3的表达,但未达到统计学意义,其中的机制有待进一步的深入研究?     

支气管哮喘合并过敏性鼻炎的流行病学调查及相关性分析

目的了解南京地区支气管哮喘患者合并过敏性鼻炎的情况,计算支气管哮喘患者中过敏性鼻炎的发生率,并分析过敏性鼻炎与支气管哮喘在临床表现方面的相关性。方法问卷调查南京地区134例支气管哮喘患者,详细了解其临床表现及治疗现状,建立相应的个人数据库档案,对数据进行统计学分析。结果134例支气管哮喘患者中,82例(61.2%)并发过敏性鼻炎,过敏性鼻炎和支气管哮喘的发病年龄及病程间的差异无统计学意义(P>0.10)。82例患者中,哮喘严重程度一级(轻度间歇)56例,二级(轻度持续)21例,三级(中度持续)4例,四级(重度持续)1例。过敏性鼻炎分型:间歇性65例,持续性17例;按严重程度分级:轻度63例,中-重度19例。所有患者中,42例(31.3%)直系三代内有气道炎症相关性疾病家族史。结论南京地区支气管哮喘合并过敏性鼻炎的发生率较高,两者临床表现相关,分型、分级具有高度一致性。     

地塞米松对慢性哮喘小鼠肺组织中白细胞介素21、磷酸化信号转导及转录激活因子3的干预作用

目的研究慢性哮喘小鼠肺组织白细胞介素21（IL-21）、磷酸化信号转导及转录激活因子3（p-STAT3）表达变化,探讨地塞
米松对小鼠肺组织IL-21、p-STAT3表达的影响。方法SPF级BALB/C雌性小鼠33只,随机分为对照组、哮喘组、地塞米松治疗
组,每组11只。卵清白蛋白(OVA)致敏和激发建立哮喘小鼠模型;肺泡灌洗液进行细胞计数和分类;HE染色观察气道炎症程度;
免疫组化法观察IL-21和p-STAT3在小鼠肺组织的表达;免疫蛋白印迹法分析小鼠肺组织中IL-21、p-STAT3蛋白的表达。结果
哮喘组肺泡灌洗液中的细胞总数和嗜酸性粒细胞计数较对照组和地塞米松组明显增加( P<0.01);哮喘组小鼠肺组织IL-21蛋
白、p-STAT3蛋白的表达高于对照组（P<0.05）,地塞米松组IL-21蛋白、p-STAT3蛋白的表达低于哮喘组（P<0.05）。结论地塞米
松抑制了慢性哮喘小鼠模型IL-21、p-STAT3的表达,IL-21/STAT3细胞信号通路可能为地塞米松治疗哮喘的作用机制之一。
     

过敏性哮喘患者外周血细胞因子水平变化及临床意义

目的：探讨细胞因子IL‐17、IL‐22和IL‐10在过敏性哮喘患者外周血中的变化及临床意义。方法选取过敏性哮喘患者40例（哮喘组）和健康体检者30例（对照组）,采用ELISA法检测外周血培养上清中IL‐17、IL‐22和IL‐10的表达;电化学发光免疫分析法检测血清中Ig E的水平,全自动血液分析仪检测全血嗜酸性粒细胞比率;IL‐17、IL‐22和IL‐10与哮喘严重程度进行Pearson相关性分析。结果哮喘组血清中IgE的水平及全血嗜酸性粒细胞比率高于对照组（P＜0．05）;哮喘组外周血IL‐17、IL‐22水平高于对照组,而IL‐10水平低于对照组（P＜0．05）;哮喘严重程度与IL‐17、IL‐22水平呈正相关（P＜0．01）,而与IL‐10水平呈负相关（ P＜0．05）。结论 IL‐17、IL‐22和IL‐10在过敏性哮喘的发病机制中起重要作用,动态监测其变化有利于临床诊断及治疗。