抗细胞间粘附分子-1单克隆抗体在过敏性气道炎症中的作用

目的：探讨抗细胞间粘附分子－1（ICAM－1）单克隆抗体（单抗）对抗原引起的气道炎症的影响,加深认识ICAM－1在支气管哮喘发病机制中的作用。方法：应用鸡卵清蛋白致敏和刺激小鼠以诱导哮酸性粒细胞（EOS）聚集到气道,收集支气管肺泡灌洗液（BALF）细胞并检测ICAM－1分子的表达水平,观察静注抗ICAM－1单抗后BALF中EOS数以及白细胞介素－4（IL－4）水平的变化,结果：小鼠经抗原致敏和刺激后BALF中可以见到大量的EOS,经抗ICAM－1单抗处理后EOS数降低了63％,抗ICAM－1单抗可抑制肺组织IL－4的产生。结论：抗ICAM－1单抗能够抑制气道EOS浸润,其作用机制很可能与抑制局部IL－4的产生有关,提示抑制气道抗原呈递细胞的活性有利于哮喘的治疗。     

氧化苦参碱对哮喘小鼠抗炎作用的研究

目的：探讨氧化苦参碱治疗哮喘的抗炎作用机制及其对白细胞介素－4（IL－4mRNA)表达的影响。方法：建立小鼠哮喘模型，观察氧化苦参碱对哮喘小鼠支气管肺泡灌洗液中炎性细胞、肺组织病理的改变；应用半定量反转录－聚合酶链反应检测肺组织IL－4mRNA表达的变化。结果：氧化苦参碱可显著减轻哮喘小鼠气道及肺组织中哮酸性细胞的浸润，显著抑制哮喘小鼠肺组织中IL－4mRNA的表达水平。结论：氧化苦参碱对哮喘小鼠有明显的抗气道变应性炎症及抑制IL－4mRNA表达的作用。     

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)为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。     

抑制树突状细胞的自噬改善小鼠哮喘病情

目的 研究抑制树突状细胞(DCs)自噬对DCs功能及小鼠哮喘的影响.方法 (1)将BALB/c小鼠按随机数字表法分为3组:急性哮喘对照组(哮喘组)、哮喘自噬抑制剂氯喹(CQ)治疗组(CQ组)和空白对照组(对照组).哮喘组和CQ组利用卵清蛋白(OVA)诱导建立小鼠过敏性哮喘模型,CQ组加用CQ.用H-E染色观察各组小鼠肺组织的病理改变,酶联免疫吸附实验、蛋白质印迹实验、流式细胞术分别检测各组小鼠血清OVA特异性IgE以及肺DCs自噬水平、表面共刺激分子和主要组织相容性复合体Ⅱ类分子(MHCⅡ)的表达水平.(2)体外用自噬抑制剂3-甲基腺嘌呤(3MA)抑制C57/B6小鼠骨髓源DCs自噬,检测DCs表面共刺激分子、MHCⅡ的表达水平.(3)获取OT2小鼠脾脏CD4+T淋巴细胞,与各组肺DCs以1∶10的比例混匀,流式细胞术检测T细胞的增殖情况与活化反应.结果 (1)CQ组IgE的表达水平(P＜0.05)、肺炎症细胞浸润程度以及肺DCs自噬水平(P＜0.05)和CD86、MHCⅡ表达水平(P＜0.05)均低于哮喘组.(2)3MA体外抑制骨髓源DCs自噬后,DCs表面的CD86及MHCⅡ表达均低于哮喘组(P＜0.05).(3)CQ组肺DCs体外诱导的T细胞增殖能力与活化反应均弱于哮喘组(P＜0.05).结论 自噬抑制剂可抑制过敏性哮喘肺DCs的自噬,下调DCs表面共刺激分子、MHCⅡ的表达以及DCs诱导的T细胞增殖能力,改善哮喘病情.     

TH细胞活性增强与支气管哮喘

传统上，根据T淋巴细胞膜表面抗原差异，分成CD4十细胞和CD8 细胞。TH细胞为CD4十细胞，根据其产生淋巴因子的差异，可进一步分为两种功能性亚群：TH1能产生白介素-2（IL－2）和Y干扰素（IFN－Y）；TH2能分泌IL－4和IL－5等。已经发现，哮喘患者的气道粘膜中，含有大量属于CD4十的m细胞，且往往处于活化状态，表现为IL－ZR阳性，细胞内存在IL－SllffoA，而正常对照组则为阴性。而且IL－5mRNA阳性程度与病人气道内活化的T细胞、嗜酸性粒细胞（EC）数量相关。此外，与对照组相比，哮喘患者支气管肺泡洗洗液中IL－4、IL－5…     

肉苁蓉多糖的纯化及其对T细胞功能调节的研究

研究肉苁蓉主要成分之—─—多糖对小鼠胸腺T细胞的功能调节。方法：采用沉淀法获肉苁蓉粗多糖，以DEAE－SephadexA－50和SephacrylS－200柱层析，获得肉苁蓉多糖（CDPS）。再采用噻唑蓝比色法（MTT）观察CDPS对小鼠脾、胸腺淋巴细胞增殖反应的影响及对正常小鼠脾淋巴细胞分泌IL－2的影响。结果：CDPS纯化后经SephacrylS－200鉴定为单一对称峰。CDPS体外实验，在12．5～200μg／ml浓度范围内，有单独和协同ConA、PHA促进小鼠胸腺淋巴细胞增殖的作用（P＜0．01）。CDPS在100μg／ml浓度时，能显著提高小鼠脾淋巴细胞分泌IL－2的能力．其IL－2活性明显高于对照组（P＜0．01）。结论：肉苁蓉多糖能增加小鼠脾、胸腺淋巴细胞的增殖反应，且与ConA、PHA有协同刺激小鼠胸腺淋巴细胞增殖的作用；并能显著提高小鼠脾脏T淋巴细胞分泌IL－2。     

哮喘病人外周血单个核细胞ICAM-1 mRNA表达测定

目的：探讨细胞间粘附分子－1（ICAM－1）在哮喘炎症反应中的作用，进一步了解哮喘发病机制。方法：采用免疫组织化学和RT－PCR方法检测10例支气管哮喘发作患者和10例正常人外周血单个核细胞（PBMCs)ICAM-1表达。结果：哮喘患者PBMCs ICAM-1及ICAM－1mRNA均较正常对照组增高（P＜0．05），哮喘患者PBMCs ICAM－1与ICAM－1 mRNA表达成正相关。结论：ICAM－1参与哮喘炎症反应的发生。     

大枣中性多糖对小鼠脾淋巴细胞增殖的影响

目的 研究大枣中性多糖（JDP－N）对小鼠脾细胞增殖作用及其对刀豆素A（ConA)活化脾细胞内游离Ca^2 浓度（[Ca^2 ]i)的影响。方法 采用MTT法测定增殖程度,用激光扫描共聚焦显微镜技术测定细胞内[Ca^2 ]i。结果 JDP－N能促进小鼠脾细胞自发增殖反应和混合淋巴细胞培养反应,但对经ConA活化、IL－2诱导的脾细胞无促进增殖作用,且对ConA活化的脾细胞内[Ca^2 ]i无影响。结论 JDP－N仅对未活化的小鼠脾细胞有促进增殖作用。     

n⁃3多不饱和脂肪酸对NOD小鼠T细胞的免疫调节作用

目的：探讨n?3多不饱和脂肪酸（n?3 poly unsaturated fatty acid,n?3 PUFA）对NOD小鼠T细胞免疫学功能的影响。 方法： 野生型Balb/c小鼠和已出现典型的Ⅰ型糖尿病症状的NOD小鼠脾 细胞,磁珠分选后获得小鼠CD4+ T细胞,将其分 为4组：野生型 鼠为Wild type组;NOD小鼠分为未处理组、二十二碳六烯 （docosahexaenoic acid,DHA）处理组、二十碳五烯酸（eicosapentaenoic acid,EPA）处理组。DHA、EPA处理24h,PMA和Ionomycin刺激活化后,采用CCK?8法检测T细胞增殖 流式细胞仪检测Th1/Th2极化、ELISA法检测T细胞细胞因子的分 水平变化。结果：DHA、EPA对T细胞增殖具有显著抑制作用,促 NOD小鼠Th2细胞分化,抑制Th1细胞分化,经ELISA检测,DHA EP 能够抑制T细胞IL?6、IL?17的分泌。结论：n?3多不 饱和脂肪酸 过抑制T细胞增殖,平衡Th1/Th2比例和抑制IL?6、IL?17的分泌对NOD小鼠的T淋巴细胞起到免疫抑制作用。     

CpG脱氧寡核苷酸对抗原致敏性小鼠气道反应的影响

目的：探讨以非甲基化胞嘧啶－鸟嘌呤（CpG)脱氧寡核苷酸（ODN）治疗支气管哮喘的免疫抑制作用。方法：以卵白蛋白（OVA）免疫C57BL／6小鼠建立支气管哮喘模型,致敏阶段腹腔注射CpG oDN,以不含CpG序列的ODN及生理盐水作对照,观察应用CpG ODN对支气管哮喘形成,气道过敏性免疫反应的影响,结果：应用CpG ODN组与对照组相比：（1）明显抑制抗原激发后气道内嗜酸粒细胞的浸润（P＜0．01）;（2）明显抑制肺内IL－4,IL－5产生,增加IL－12,IFN－γ的产生;（3）明显抑制抗原诱导的气道反应性的增高;（4）明显抑制外周血总IgE及抗原特异性IgE的水平。结论：致敏阶段应用CpG ODN对抗原诱导的气道过敏反应有明显的抑制作用,可阻断支气管哮喘的形成,这种抑制作用与IL－12,IFN－γ的产生增加相关。     

The attenuative effect of purified protein derivative sensitization on T helper 2 reaction and eosinophil infiltration of the lung in ovalbumin sensitized mice

OBJECTIVE To identify the effects of tuberculin purified protein derivative (PPD) sensitization on attenuating pulmonary T helper 2 (Th2) reaction and eosinophil infiltration in ovalbumin sensitized mice, and to search for the possibility of its clinical use in the management of asthma in a new way.

METHODS Sixty C57BL/6 mice were sensitized with PPD and then with ovalbumin and aluminum hydroxide, and randomized into 4 groups: ovalbumin (OVA), pre-PPD, post-PPD and control groups. Aerosol PPD were administered 3 h before or after ovalbumin challenge in the pre-PPD and post-PPD groups respectively, and control group received aerosol PPD only. IL-4, IL-5 expression was detected by immunocytochemistry in situ hybridization. Lung slides were stained with eosin and hemotoxylin, and pathological changes were observed.

RESULTS Ovalbumin aerosol inhalation caused a mixed inflammatory infiltration dominated by CD4+ T lymphocytes and eosinophils in the lung of sensitized mice. 87.5%-89.7% and 89.0%-89.2% of the CD4+ T lymphocytes were IL-4 mRNA+ and IL-5 mRNA+ respectively. 88.7%-91.2% of IL-4 mRNA+ cells and 89.8%-90.6% of IL-5 mRNA+ cells were CD4+ T lymphocytes in OVA group. Aerosol administration of PPD markedly suppressed IL-4 and IL-5 expression, and lung eosinophil infiltration. It was more effective in pre-PPD group. 76.6%-78.0% of IL-4 mRNA+ and 73.8%-79.7% of IL-5 mRNA+ cells were CD4+ and 78.1%-84.9% and 78.4%-85.3% of the CD4+ cells were IL-4 mRNA+ or IL-5 mRNA+ respectively in pre-PPD group, both were markedly lower than that of OVA group. CD4+ percentage of IL-4 mRNA+ and IL-5 mRNA+ cells were 80.7%-82.0% and 78.0%-83.9% in post-PPD group, which were markedly lower than that of OVA group.

CONCLUSIONS Sensitization with PPD by intraperitoneal injection and then challenged by PPD inhalation markedly suppressed IL-4, IL-5 expression and eosinophil infiltration, and attenuated pulmonary Th2 reaction in ovalbumin sensitized mice. This induces Th1 type reaction and inhibits Th2 cell differentiation. It may be beneficial for glucocorticoids dependent or resistant patients.

     

Aerosol administration of dexamethasone and methotrexate attenuated Th2 reaction and eosinophil infiltration of the lung in ovalbumin sensitized mice

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百日咳蛋白对小鼠过敏性哮喘模型的免疫调节作用

目的：观察百日咳杆菌蛋白对致敏小鼠气道炎症、气道高反应性以及IFN-γ／IL-4平衡的调节作用。方法：致敏小鼠，卵白蛋白反复攻击后静脉注射乙酰甲胆碱（Mch），测定气道反应性；收集支气管肺灌洗液（BALF），检测炎症细胞及IL-4、IFN—γ水平，进行肺组织病理学检查。结果：肌注或滴鼻给予百日咳杆菌蛋白，能抑制致敏小鼠肺阻力及肺动态顺应性变化，上调肺泡灌洗液中IFN-γ／IL-4比例，降低嗜酸性粒细胞聚集，并且作用呈现剂量依赖性。病理学检查显示，百日咳杆菌蛋白能够有效抑制致敏小鼠气道上皮杯状细胞增生及肺组织中炎症细胞浸润。结论：百日咳杆菌蛋白能有效抑制过敏性哮喘小鼠肺部炎症、改善肺功能，对防治哮喘具有潜在的应用前景。     

Brg1通过STAT6促进哮喘气道黏液高分泌

目的研究染色质重构复合物核心催化亚基（Brg1）对哮喘小鼠气道黏液高分泌的影响及其作用机制。方法将6~8周龄 雌性野生型C57bl/6小鼠和Brg1-/-小鼠（Ⅱ型肺泡上皮细胞AEC2s上特异性条件敲低Brg1的C57bl/6小鼠）随机分为4组：正常 对照组、哮喘组、Brg1敲低对照组（Brg1-/-）和Brg1敲低后构建哮喘模型组（Brg1-/-+哮喘）,每组10只。哮喘组和Brg1-/-+哮喘组用 鸡卵清蛋白（OVA）制备过敏性哮喘模型,对照组用生理盐水代替。收取标本,用ELISA检测小鼠支气管肺泡灌洗液（BALF）中 黏蛋白MUC5AC和IL-13的表达。糖原染色检测小鼠气道杯状细胞的增生和黏液分泌,q-PCR和免疫组化检测各组小鼠气道 黏蛋白MUC5AC的表达和定量。Western blot检测各组小鼠肺组织中STAT6、p-STAT6的表达。结果Brg1-/-+哮喘组较哮喘组 气道杯状细胞增生和黏液分泌均显著减少,BALF中IL-13、MUC5AC表达明显降低,肺组织MUC5AC mRNA表达显著降低, 同时肺组织STAT6和磷酸化STAT6显著下调。结论Brg1-/-敲低的小鼠建立哮喘模型时气道黏液分泌较野生型小鼠减轻,其可 能通过影响STAT6从而抑制黏蛋白MUC5AC的表达,抑制支气管哮喘气道黏液高分泌,表明Brg1具有促进哮喘气道黏液高分 泌的作用。     

Linker for activation of T cells contributes to airway inflammation in an asthmatic mouse model

Background Allergic asthma is associated with airway inflammation and hyperresponsiveness caused by dysregulated production of cytokines secreted by allergen-specific helper T-type 2 （Th2） cells. The linker for activation of T cells （LAT） is a membrane-associated adaptor protein, which has been shown to take part in regulating T cell receptor （TCR） signaling and T cell homeostasis. In this study, we established an asthmatic mouse model to examine the changes in LAT levels during allergic airway disease and the effects of LAT transgenic expression on airway inflammation. Methods T cells from mouse lung tissues were isolated from allergen challenged （ovalbumin （OVA）） and control mice, and the purity of these isolated T cells was examined by fluorescence-activated cell sorter （FACS）. Semi-quantitative RT-PCR and Western blotting were used to detect the expression of the LAT gene and LAT protein, respectively. After an intranasally administered mixture of pCMV-HA-LAT plasmid and Lipofectamine 2000, 24 hours before and 72 hours after allergen challenge, the BALF cell count and the differential cytologies were studied. In addition, IL-4 and IFN-γ levels in the BALF were determined by ELISA, and pathological changes in lung tissues were observed. Results LAT protein and mRNA expression were decreased in lung T cells in a mouse model of allergen-induced airway disease. After intranasal administration of pCMV-HA-LAT, histopathological examination of the lungs showed that intervention with LAT overexpression prevented mice from developing airway inflammation, and the number of total cells, eosinophils, neutrophils, and lymphocytes in the BALF was reduced significantly compared with the OVA sensitized and challenged group. In addition, the Th2 cytokine IL-4 decreased, while the Thl cytokine IFN-γ increased compared to the OVA sensitized and challenged group or the OVA sensitized group plus pCMV-HA treatment. Conclusion This study demonstrates that LAT might effectively diminish Th2 cytokine responses, lung histopathological changes and lung inflammation to allergen challenge in a model of expedmentally induced asthma.     

表没食子儿茶素没食子酸酯对肥胖型哮喘小鼠气道 炎症和Treg/Th17免疫平衡的影响

目的：探讨表没食子儿茶素没食子酸酯（EGCG）对肥胖型哮喘小鼠调节性T淋巴细胞/辅助性T淋巴细胞17（Treg/Th17）免疫失衡的调节作用,为EGCG治疗肥胖型哮喘提供依据。方法：40只C57BL/6J小鼠分为正常对照组（采用正常饲料喂养）、肥胖组（采用高脂饲料喂养）、肥胖型哮喘组[采用高脂饲料喂养的同时给予卵白蛋白（OVA）致敏和激发,制备肥胖型哮喘模型],EGCG干预组（在OVA激发前1 h给予20 mg·kg^-1EGCG腹腔注射）和地塞米松干预组（在OVA激发前1 h给予2 mg·kg^-1地塞米松腹腔注射）,每组8只。采用无创肺功能仪测定各组小鼠的增强呼气间歇（Penh）值;HE染色观察各组小鼠肺组织病理形态表现,HE染色切片半定量方法进行小鼠气道炎症评分; ELISA法检测各组小鼠血清中脂联素、瘦素和支气管肺泡灌洗液（BALF）中白细胞介素10（IL-10）、白细胞介素17A （IL-17A）水平;流式细胞术检测各组小鼠脾组织中Th17和Treg百分比。结果：肥胖组小鼠体质量高于正常对照组（P<0.05）,为正常对照组小鼠平均体质量的1.67倍。与正常对照组比较,肥胖型哮喘组小鼠Penh值和气道炎症评分均升高（P<0.05）,血清中瘦素水平升高（P<0.05）,BALF中IL-17A水平升高（P<0.05）,IL-10水平降低（P<0.05）,脾组织中Th17百分比升高（P<0.05）,Treg百分比降低（P<0.05）。与肥胖型哮喘组比较,EGCG干预组小鼠Penh值和气道炎症评分均降低（P<0.05）,血清中瘦素水平降低（P<0.05）,BALF中IL-17A水平降低（P<0.05）,BALF中IL-10水平升高（P<0.05）,脾组织中Th17百分比降低（P<0.05）,脾组织中Treg百分比升高（P<0.05）。结论：在肥胖型哮喘小鼠中存在Treg/Th17免疫失衡,EGCG能够抑制肥胖型哮喘小鼠的气道炎症及气道高反应性,能够改善Treg/Th17免疫失衡。     

实验性支气管哮喘气管、支气管、肺形态学变化的实验研究

目的 :探讨实验性支气管哮喘时气管、支气管、肺的形态学变化。方法 :采用卵蛋白致敏豚鼠 ,取气管支气管肺石蜡切片。H -E和甲苯胺蓝染色。结果 :气管支气管粘膜下淋巴组织增生 ,肺门淋巴结肿大 ,粘膜水肿、杯状细胞增多。管壁可见许多嗜酸性粒细胞、中性粒细胞、淋巴细胞浸润。结论 :支气管哮喘是以嗜酸性粒细胞为主的气道慢性炎症性疾病     

Effects of glucocorticoid and cysteinyl leukotriene 1 receptor antagonist on CD34+ hematopoietic cells in bone marrow of asthmatic mice

Background Corticosteroids remain the most effective therapy available for asthma. They have widespread effects on asthmatic airway inflammation. However, little is known about the effects of corticosteroids on the production of bone marrow inflammatory cells in asthma. This study observed the effects of glucocorticoid and cysteinyl leukotriene 1 receptor antagonist on CD34+ hematopoietic cells, so as to explore the possible effectiveness of a bone marrow-targeted anti-inflammatory strategy. Methods Balb/c mice were sensitized and challenged with ovalbumin (OVA) to establish an asthmatic model. For two consecutive weeks, asthmatic mice were challenged with OVA while being given either prednisone, montelukast, prednisone plus montelukast, or sterile saline solution. The mice were killed 24 hours after the last challenge with OVA, and bronchoalveolar lavage fluid (BALF), peripheral blood, and bone marrow were collected. Eosinophils in peripheral blood and BALF, and nucleated cells in BALF, peripheral blood, and bone marrow were counted. The percentages of CD34+ cells, CD4+ T lymphocytes and CD8+ T lymphocytes among nucleated cells in peripheral blood and bone marrow were counted by flow cytometry. Immunocytochemistry and in situ hybridization were employed to detect expression of CD34 and interleukin (IL)-5Rα mRNA (CD34+ IL-5Rα mRNA+ cells) among bone marrow hematopoietic cells. Results Compared with the sterile saline solution group, the number of eosinophils in BALF and peripheral blood, CD34+ cells in peripheral blood and bone marrow, and CD34+ IL-5Rα mRNA+ cells in bone marrow of mice from the prednisone and prednisone plus montelukast groups were significantly lower （P&lt;0.01）. The number of eosinophils in BALF from the montelukast group was also significantly lower （P&lt;0.05）. Conclusions The results suggest that, in this asthmatic mouse model, prednisone probably inhibits proliferation, differentiation, and migration of CD34+ cells in bone marrow, blocks eosinophilopoiesis in bone marrow, and interferes with eosinophil migration into peripheral blood and subsequent recruitment in the airway. In addition, montelukast may suppress eosinophil infiltration into the lungs of asthmatic mice. However, a significant inhibitory effect of montelukast on the proliferation and migration of CD34+ cells and a cooperating effect with prednisone on bone marrow of asthmatic mice were not observed.     

Small interfering RNA-mediated knockdown of Notchl in lung T cells of asthmatic mice affects T cell differentiation

Background The immunologic response to allergens mediated by T lymphocytes is an incipient key element in the pathogenesis of asthma,and Th1/Th2 balance is regarded as the core of asthma pathogenesis.Notch is a single-pass transmembrane receptor protein that regulates differentiation,proliferation and apoptosis in a broad range of cells.It is considered that the Notch signal pathway works in every stage of T cell development and differentiation.Whether the pathway of asthma pathogenesis is related to Notch1 remains unknown.This study is aimed to investigate whether the pathway of asthma pathogenesis is related to Notch1 by examining the effect of knockdown of the Notch1 gene by small interfering RNA on T cell differentiation.Methods An OVA-induced asthma mouse model was established.The expression of Notch1 in the tissue and T cells of the lung from asthmatic mice was detected by RT-PCR and Western blotting.The expression of Notch1 and cytokine interleukin(IL)-4 and interferon(IFN)-γ in activated lung T cells was detected by RT-PCR and enzyme-linked immunosorbent assay after blocking Notch1 by small interfering RNA.Results The mRNA and protein expression of Notch1 increased significantly both in the lung tissue and lung T cells of asthmatic mice(both P＜0.05).IL-4 decreased and IFN-γ increased significantly in active lung T cells after Notch1 was blocked by Notch1-specific small interfering RNA(IL-4:(2.51±0.51)pg/ml vs 0.64±0.27)pg/ml protein;IFN-γ:(21.72±4.24)pg/ml vs(39.79±4.09)pg/ml protein,P＜0.05).Conclusion This study demonstrated that the Notch1 signal might play a role in the pathogenesis of asthma by its involvement in Th1/Th2 differentiation.