Foxp3~+ Treg、Th细胞迁移及ET-1与佐剂关节炎大鼠模型肺功能的关系

目的:观察佐剂关节炎(Adjuvant arthritis,AA)大鼠肺功能降低与辅助T细胞(Th)、调节T细胞(Treg)及Foxp3的关系。方法:将SD大鼠随机分为正常对照(NC)组和模型对照(MC)组,每组15只,向MC组大鼠右后足跖皮内注射弗氏完全佐剂0.1 ml致炎,复制成AA模型。致炎48 d后,采用小动物肺功能仪检测肺功能,酶联免疫吸附法检测内皮素(ET)-1、白细胞介素(IL)-10、γ干扰素(IFN-γ),免疫组化法检测肺组织IL-1β、IL-10表达,流式细胞仪测定Treg的表达,采用PCR与免疫印迹检测肺组织Foxp3表达。结果:与NC组相比,MC组大鼠IFN-γ、ET-1、IL-1β升高;肺功能参数50%肺活量的最大呼气流量(FEF50)、75%肺活量的最大呼气流量(FEF75)、最大呼气中期流量(MMF)、用力最大呼气流量(PEF)降低,IL-10、CD4+CD25+Foxp3+Treg、Foxp3表达降低(P<0.05或P<0.01);相关分析显示,AA大鼠肺功能参数FEF75、MMF分别与IFN-γ、Th1/Th2、IL-1β呈负相关,FEF50、PEF与ET-1呈负相关;PEF、FEF75分别与IL-10、Foxp3 mRNA、Foxp3蛋白呈正相关,FEF75与CD4+CD25+Foxp3+Treg呈正相关(P<0.05或P<0.01)。结论:AA大鼠肺功能下降可能是佐剂致炎后Th细胞分泌紊乱、细胞因子失衡、内皮细胞增多,使肺组织Foxp3表达抑制,进而CD4+CD25-T细胞转化成CD4+CD25+Treg受阻,最终导致RA肺功能降低。     

佐剂性关节炎大鼠肺功能变化与Th1/Th2细胞、调节性T细胞的相关性研究

目的:探讨细胞因子、Th1/Th2细胞及调节性T细胞(Treg)、转录因子Foxp3在佐剂性关节炎(AA)大鼠肺功能损害中的作用机制。方法:将24只Wistar大鼠随机分为正常对照(NC)组和模型(Model)组,每组12只,向Model组大鼠右后足跖皮内注射弗氏完全佐剂0.1mL致炎,复制成AA模型。致炎48d后,观察两组大鼠足跖肿胀度(E)及关节炎指数(AI),HE染色观察肺组织病理学改变,计算两组大鼠肺系数(LI)、肺泡炎积分,免疫组化染色法检测Foxp3、TGF-β1蛋白表达情况。通过小动物肺功能仪检测肺功能,ELISA法测定细胞因子的变化,流式细胞术(FCM)测定Treg的表达。结果:与NC组相比,Model组大鼠E、AI、LI、1s内平均呼气流量(FEV1/FVC%)、肺泡炎积分、血清TNF-α、Th1/Th2、肺组织TGF-β1、CD4+ CD25- T细胞的表达水平明显升高,且两者差异有统计学意义(P<0.05或P<0.01);用力肺活量(FVC)、25%肺活量的最大呼气流量(FEF25)、50%肺活量的最大呼气流量(FEF50)、75%肺活量的最大呼气流量(FEF75)、最大呼气中期流量(MMF)、用力最大呼气流量(PEF)、肺动态顺应性(Cldyn)、血清IL-10、CD4+ Treg、CD4+ CD25- Treg、肺组织Foxp3蛋白表达水平显著降低(P<0.01)。Spearman相关分析结果显示,AA大鼠肺功能参数分别与E、AI、TNF-α、IL-10、Th1/Th2及CD4+ Treg、CD4+CD25+Treg、CD4+ CD25- T细胞、Foxp3、TGF-β1表达呈相关性,且相关有统计学意义(P<0.05或P<0.01)。结论:大鼠在致炎后对抗原刺激呈高敏反应状态,Th1/Th2状态失衡、CD4+ CD25- T细胞转化成CD4+ CD25+ Treg受阻,免疫调节功能紊乱,释放大量细胞因子和炎症介质,导致局部关节的病变和肺组织损害,从而发生AA肺功能降低。     

佐剂性关节炎大鼠肺功能变化与Foxp3、TGF-β1/Smads信号传导通路的相关性研究

目的:观察佐剂性关节炎(Adjuvant arthritis,AA)大鼠肺系数、肺功能变化、调节性T细胞及Foxp3、TGF-β1、Smad3、Smad7蛋白表达,探讨Foxp3与TGF-β/Smads信号传导通路在佐剂性关节炎大鼠肺功能降低中的可能作用机制。方法:将24只Wistar大鼠随机分为正常对照组和模型组,每组12只,向模型组大鼠右后足跖皮内注射弗氏完全佐剂0.1 ml致炎,复制成佐剂性关节炎模型。致炎48天后,观察两组大鼠足跖肿胀度及关节炎指数(AI),计算两组大鼠肺系数,检测大鼠肺功能,测定调节性T细胞百分率,HE染色观察肺病理学改变,免疫组化染色观察Foxp3、TGF-β1、Smad3、Smad7蛋白表达情况。结果:①与正常对照组相比,AA模型组大鼠足跖肿胀度、AI、肺系数、1秒内平均呼气流量(FEV1/FVC)、肺泡炎积分、TGF-β1及Smad3蛋白表达明显升高(P0.01);用力肺活量(FVC)、25%肺活量的最大呼气流量(FEF25)、50%肺活量的最大呼气流量(FEF50)、75%肺活量的最大呼气流量(FEF75)、最大呼气中期流量(MMF)、用力最大呼气流量(PEF)、肺动态顺应性(Cldyn)、CD4+T细胞、CD25+T细胞、CD4+CD25+T细胞百分率、Foxp3蛋白及Smad7蛋白表达显著降低(P0.01)。②Spearman相关分析可知,AA大鼠肺功能参数中FEF50、MMF与足跖肿胀度呈负相关,MMF与肺系数呈负相关,Cldyn与TGF-β1蛋白积分光密度值呈负相关;FEF50、MMF与关节炎指数呈正相关,FEF75与肺系数呈正相关,FEV1/FVC与Foxp3蛋白表达染色指数、Foxp3蛋白积分光密度值呈正相关(P0.05或P0.01)。结论:AA大鼠在足跖肿胀度、关节炎指数升高的同时出现肺功能的下降,提示可能是致炎后炎症的持续、发展而出现慢性炎症反应导致肺的损伤(肺间质纤维化),而肺功能的下降与Foxp3、Smad3、Smad7、TGF-β1蛋白表达呈相关性,说明转录因子Foxp3和TGF-β1/Smads信号传导通路共同参与其作用机制。     

新风胶囊通过调节肺泡Ⅱ型上皮细胞Notch/Jagged-HES轴改善佐剂性关节炎大鼠肺功能北大核心CSCD

目的观察新风胶囊(XFC)对肺泡Ⅱ型上皮细胞Notch/Jagged/HES影响。方法大鼠分为正常对照组、模型组、来氟米特(LEF)组、XFC组,除正常对照组外,其余3组复制佐剂关节炎大鼠模型。致炎后第13天给药,每天1次,连续给药30 d。正常对照组、模型组给予生理盐水灌胃,每天1次;LEF组给予LEF(0.5 mg/100 g)灌胃、XFC组给予XFC(0.034 g/100 g)灌胃,观察大鼠足跖肿胀度、关节炎指数、肺功能,透射电镜观察大鼠肺泡Ⅱ型上皮细胞超微结构,Western blot法检测肺泡Ⅱ型上皮细胞转化生长因子β1(TGF-β1)、Notch1、Notch3、Jagged1、HES1蛋白表达。结果模型组大鼠肺功能参数最大呼气第一秒呼出的气量的容积(FEV1)、50%肺活量的呼气流量(FEF50)、75%肺活量的呼气流量(FEF75)、用力最大呼气流量(PEF)较NC组显著降低,肺泡Ⅱ型上皮细胞超微结构破坏,肺泡Ⅱ型上皮细胞TGF-β1、Notch1、Notch3、Jagged1、HES1表达升高。与模型组比较,XFC组FEV1、FEF_(50)、FEF_(75)、PEF均显著升高,TGF-β1、Notch1、Notch3、Jagged1、HES1降低。XFC组较LEF组肺功能升高。结论 XFC通过下调TGF-β1、Notch1、Notch3、Jagged1、HES1,抑制肺间质纤维化,改善肺功能。     

佐剂关节炎大鼠肺功能降低与调节性T细胞减少及Foxp3表达下调相关

目的 观察佐剂关节炎(AA)大鼠肺功能、调节性T细胞(Treg)及其表面标志物-叉头状转录因子(Foxp3)变化,探讨Treg、Foxp3在RA肺病变中的作用.方法 将30只大鼠随机分为正常组和模型组,每组15只,向模型组大鼠右后足跖皮内注射弗氏完全佐剂0.1 mL致炎,复制成AA模型.致炎30 d后,观察大鼠足跖肿胀度、关节炎指数,采用动物肺功能仪检测大鼠肺功能,流式细胞术检测大鼠外周血Treg表达,RT-PCR、免疫组化、免疫印迹法检测大鼠肺组织Foxp3 mRNA、Foxp3蛋白表达.结果 与正常组比较,AA大鼠组织肿胀度和关节炎指数升高,肺功能参数降低,外周血CD4+ CD25+ Treg、CD4+ CD25+Foxp3+ Treg表达降低,同时,肺组织Foxp3 mRNA和Foxp3蛋白表达水平亦降低(P＜0.01或P＜0.05).结论 AA大鼠在发生关节炎症的同时,其肺功能水平降低,Treg、Foxp3表达降低,免疫平衡失调.     

基于Notch和PKC/NF-κB通路串话研究新风胶囊改善佐剂性关节炎大鼠肺功能机制

目的基于Notch和PKC/NF-κB通路串话研究新风胶囊(XFC)改善佐剂性关节炎大鼠(AA)肺功能的作用机制。方法 SD大鼠,随机分为正常组、模型组、新风胶囊组,来氟米特组作为阳性药物对照组,除正常组外,采用Fruend完全佐剂皮内注射复制AA大鼠模型,造模后第19天开始连续灌胃给药30 d,每天1次。实验结束后观察各组大鼠足趾肿胀度(E)、关节炎指数(AI)、肺功能、肺组织病理形态及肺组织Notch和PKC/NF-κB信号通路各基因与蛋白的变化。结果与正常组相比较,其余各组大鼠E、AI、IL-6、IL-17、肺组织Notch4、Jagged1、Jagged2、Rac-1、PKC、NF-κB蛋白及m RNA表达升高(P0.01或P0.05),IL-10、IL-35的表达是显著降低的(P0.01或P0.05);与模型组相比,新风胶囊组、来氟米特组肺功能、IL-10、IL-35显著升高(P0.01或P0.05),E、AI、IL-6、IL-17以及肺组织Jagged 1、Jagged 2、Notch 4、Rac-1、PKC-α、NF-κB p65、Notch1、delta1、HES1、PKC、NF-κB、Rac-1表达降低(P0.01或P0.05);与来氟米特组相比,新风胶囊组肺功能、IL-10、IL-35显著升高(P0.01或P0.05),IL-17、Notch1、Rac-1、delta1、Rac-1、NF-κB p65、Notch4明显降低(P0.01或P0.05),在降低Jagged1、Jagged2、PKC、NF-κB、HES1方面无明显差异。相关性分析显示:AA大鼠肺组织Notch和PKC/NF-κB信号通路之间存在相关性且肺功能参数与这2个通路也存在相关性。结论新风胶囊可能通过调节Notch和PKC/NF-κB通路的串话,抑制炎症因子的分泌,降低炎症反应和减少免疫复合物的沉积,进而改善关节症状和肺功能。     

新风胶囊通过抑制PKC/NF-κB通路改善佐剂性关节炎大鼠的肺功能北大核心CSCD

目的观察新风胶囊(XFC)对佐剂关节炎(AA)大鼠蛋白激酶C(PKC)/核因子κB (NF-κB)信号通路影响。方法将大鼠分正常对照(NC)组、模型对照(MC)组、XFC组、来氟米特(LEF)组。除NC组外,其余组采用Freund完全佐剂复制AA模型,第19天给药,每天1次,共30 d。XFC剂量为0. 34 g/(kg·d),1 m L/100 g灌胃,LEF剂量为0. 05 mg/(kg·d)灌胃;采用肺功能仪检测大鼠肺功能参数,ELISA检测血清白细胞介素6(IL-6)、IL-12、IL-10、IL-17、IL-35、基质金属蛋白酶9(MMP-9)水平,实时定量PCR检测肺组织Ras相关C3肉毒素底物1(Rac-1)、PKC、NF-κBp65 mRNA水平,Western blot法检测肺组织Rac-1、PKC、NF-κBp65蛋白水平,免疫组织化学染色法观察肺组织PKC、NF-κB的表达。结果 XFC组大鼠肺功能参数最大呼气第一秒呼出的气量的容积(FEV1)、50%肺活量的呼气流量(FEF50)、75%肺活量的呼气流量(FEF75)、用力最大呼气流量(PEF)较MC组显著升高,XFC组大鼠血清IL-10、IL-35水平升高,血清IL-6、IL-17、MMP-9降低,肺组织PKC、NF-κBp65、Rac-1 mRNA及PKC、NF-κBp65蛋白水平降低。结论 XFC通过抑制PKC/NF-κB通路,调节相关细胞因子的平衡,改善肺功能。     

新风胶囊通过抑制PKC/NF-κB通路改善佐剂性关节炎大鼠的肺功能

目的观察新风胶囊(XFC)对佐剂关节炎(AA)大鼠蛋白激酶C(PKC)/核因子κB (NF-κB)信号通路影响。方法将大鼠分正常对照(NC)组、模型对照(MC)组、XFC组、来氟米特(LEF)组。除NC组外,其余组采用Freund完全佐剂复制AA模型,第19天给药,每天1次,共30 d。XFC剂量为0. 34 g/(kg·d),1 m L/100 g灌胃,LEF剂量为0. 05 mg/(kg·d)灌胃;采用肺功能仪检测大鼠肺功能参数,ELISA检测血清白细胞介素6(IL-6)、IL-12、IL-10、IL-17、IL-35、基质金属蛋白酶9(MMP-9)水平,实时定量PCR检测肺组织Ras相关C3肉毒素底物1(Rac-1)、PKC、NF-κBp65 mRNA水平,Western blot法检测肺组织Rac-1、PKC、NF-κBp65蛋白水平,免疫组织化学染色法观察肺组织PKC、NF-κB的表达。结果 XFC组大鼠肺功能参数最大呼气第一秒呼出的气量的容积(FEV1)、50%肺活量的呼气流量(FEF50)、75%肺活量的呼气流量(FEF75)、用力最大呼气流量(PEF)较MC组显著升高,XFC组大鼠血清IL-10、IL-35水平升高,血清IL-6、IL-17、MMP-9降低,肺组织PKC、NF-κBp65、Rac-1 mRNA及PKC、NF-κBp65蛋白水平降低。结论 XFC通过抑制PKC/NF-κB通路,调节相关细胞因子的平衡,改善肺功能。     

风湿病患者肺功能降低与BTLA阳性细胞及调节性T细胞的数量减少有关

目的探讨B、T淋巴细胞衰减因子(BTLA)、调节性T细胞(Treg)与风湿病患者肺功能降低的关系。方法选取482例风湿病患者,包括类风湿性关节炎(RA)198例,强直性脊柱炎(AS)114例、干燥综合征(SS)102例、骨关节炎(OA)68例,应用肺功能仪检测患者肺功能水平,采用流式细胞术检测患者外周血B、T淋巴细胞衰减因子(BTLA)和调节性T细胞(Treg)表达。结果与正常组比较,风湿病患者肺功能降低,外周血BTLA、Treg表达降低;与风湿病BTLA、Treg正常组比较,BTLA、Treg异常组肺功能参数第1秒用力呼气容积(FEV1)、最大呼气流量(PEF)、50%肺活量位的最大呼气流量(FEF50)、FEF75降低(P0.05或P0.01);相关分析显示,肺功能参数用力肺活量(FVC)、最大通气量(MVV)、FEV1、FEF25、FEF50分别与BTLA、Treg呈正相关,FVC、FEV1、FEF50、FEF75分别与IgA、IgM呈负相关(P0.05或P0.01)。结论风湿病患者肺功能降低可能与BTLA、Treg表达降低,促使T细胞、B细胞过度异常活化有关。     

新风胶囊通过BTLA-HVEM诱导Treg免疫耐受改善膝骨关节炎大鼠心肺功能

目的:观察膝骨关节炎(KOA)大鼠心肺功能的变化及新风胶囊(XFC)对其影响,探讨可能的分子机制.方法:按随机数字表将40只大鼠随机分为正常对照(NC)组,模型对照(MC)组,氨基葡萄糖对照(GS)组,XFC组,每组10只.除NC组外,采用关节腔注射木瓜蛋白酶和L-半胱氨酸方法复制成KOA大鼠模型,造模后第14天开始给药.NC组及MC组均给予生理盐水,剂量为0.01 g/kg,其余2组分别给予GS、XFC混悬液,剂量分别为0.098 g/kg、0.375 g/kg.采用超声诊断仪检测大鼠心功能,动物肺功能仪检测大鼠肺功能,ELISA法检测BTLA、HVEM、IL-17、IL-4、TGF-β1;流式细胞术检测大鼠外周血CD4+ CD25+Treg、CD4+ CD25+Foxp3+ Treg的表达.结果:与NC组比较,MC组体质量、E、E/A、FVC、FEV1、FEF25、FEF50、FEF75、MMF、PEF,BTLA、HVEM、IL-4、CD4+ CD25+ Treg、CD4+ CD25+ Foxp3+Treg明显降低,TGF-β1、IL-17明显升高(P＜0.01或P＜0.05).与MC组比较,各组大鼠体质量,心功能参数E峰、E/A,肺功能参数FEV1、FEF5O、FEF75、PEF,BTLA、HVEM、IL-4、CD4+ CD25+ Treg、CD4+ CD25+ Foxp3+ Treg明显升高,关节软骨Mankin评分、心系数、肺系数、TGF-β1、IL-17明显降低(P＜0.01或P＜0.05);与GS组相比,XFC组体质量、Treg升高最为明显(P＜0.01或P＜O.05).结论:新风胶囊改善KOA大鼠关节软骨Mankin评分,改善其心肺功能,其机制可能是促进BTLA-HVEM负调共刺激信号作用,诱导Treg免疫耐受,上调IL-4表达,下调IL-17、TGF-β1表达,抑制异常免疫炎症反应.     

Airway obstruction in rheumatoid arthritis: CT manifestations, correlated with pulmonary function testing

In the present study, the signs of airflow obstruction on inspiratory and expiratory CT scans in 45 patients with rheumatoid arthritis were investigated. Radiologic findings were evaluated and correlated with the clinical data, which included rheumatoid factors and pulmonary function tests results. A lung biopsy was performed in five patients. The pattern of CT findings was as follows: infiltrative (n=15), obstructive (n=12), mixed (infiltrative and obstructive; n=10), other complicating diseases (n=7), and normal (n=1). The rheumatologic factor between patients with bronchial wall thickenings and patients without thickenings was significantly different (p=0.009). The forced expiratory flow rate between 25% and 75% of the vital capacity (FEF(25-75%)) was significantly more reduced in patients with interlobular septal thickenings than in patients without these thickenings. The patients with mosaic attenuation had significantly lower mean values of FEF(25-75% ) (p=0.001) and a lower peak expiratory flow (p=0.003) than patients without mosaic attenuation. On expiratory scans, the mean air-trapping score was 21%. These air-trapping scores were found to be well correlated with FEV1/FVC (r=0.230, p=0.0452), and FEF25-75% (r=-0.63, p= 0.05). It is widely known that a relatively higher percentage of mosaic attenuation with air-trapping and a good correlation between these and functional values contribute to the detection of early airway obstruction in patients with rheumatoid arthritis, and even in patients with infiltrative lung disease only.     

The effects of hormone replacement therapy type on pulmonary functions in postmenopausal women

OBJECTIVE: To study whether hormone replacement therapy (HRT) or Tibolone has an effect on pulmonary function in postmenopausal women. METHODS: Seventy-five postmenopausal women without any risk factor for pulmonary disease were included in this randomized, prospective study. Fifty women had undergone natural menopause and 25 had had a hysterectomy/ooforectomy. Twenty-five natural menopause women were randomly allocated to two groups: 25 patients (Group I) were treated with Tibolone 2.5 mg/day, 25 patients (group II) with Estradiol Hemihidrate 2 mg+Norethindron Asetate 1 mg/day. Twenty-five induced menopause women were treated with 17 beta-estradiol 2 mg/day. Lung function tests including forced vital capacity (FVC), forced expiratory volume (FEV(1)), FEV(1)/FVC, forced expiratory flow rate over the 25-75% of the forced vital capacity volume (FEF(25-75%)), and peak expiratory flow rate (PEF) were evaluated at the beginning and 3 months after the treatment to assess the effects of HRT and Tibolone on respiratory function. RESULTS: Regardless of HRT types a significant difference was observed in FVC and FEV(1) after 3 months of the therapy (P=0.001, 0.0001, respectively). No significant difference was found between pre and post therapy values in the other parameters (P>0.05). CONCLUSIONS: We determined a significant increase in FVC and FEV(1) parameters of pulmonary functions after 3 months of the therapy regardless of HRT types. Therefore, we think that HRT regimens have modifying effects on pulmonary function in postmenopausal women.     

Spirometric reference values from a Mediterranean population

Maximal expiratory flow-volume (MEFV) curves were measured in 1044 healthy nonsmoking volunteers living in the Barcelona area, as part of a larger interhospital project to obtain reference values of pulmonary function tests. Forced vital capacity (FVC), one-second forced expiratory volume (FEV1), FEV1/FVC, %, forced maximal mid-expiratory flow (FEF25-75%), peak expiratory flow rate (PEF) and maximal expiratory flow at 50 and 75% of FVC (MEF50% and MEF25% respectively) were obtained and expressed at BTPS conditions. Techniques and equipments followed both the recommendations of the American Thoracic Society (ATS) and of the European Community for Coal and Steel (ECCS). Prediction equations for age 20 through 70 were calculated for both sexes from a final sample composed of 870 adult subjects, 443 males and 427 females. Simple linear equations using height, age and body weight predicted all spirometric variables as well as more complex equations except MEF25%. Logarithmic equations were proposed for MEF25% to correct for the heteroscedasticity shown in a simple linear model. To our knowledge, this study provides reliable spirometric equations from a large urban Mediterranean sample which were lacking so far in the literature.     

Jagged2-expressing hematopoietic progenitors promote regulatory T cell expansion in the periphery through notch signaling

Cellular interactions promoting the in vivo expansion of CD4(+)CD25(+)Foxp3(+) regulatory T (Treg) cells for maintenance of immune tolerance remain poorly defined. Here we report that mobilized Lin(-)Sca-1(+)c-kit(+) (LSK) hematopoietic progenitor cells (HPCs), unlike medullary hematopoietic stem cells (HSCs), selectively drove the direct, immediate expansion of functional host-derived Treg cells, thereby preventing the progression to overt spontaneous autoimmune diabetes in nonobese diabetic mice. Treg cell expansion required cell-to-cell contact and Notch3 signaling, which was mediated selectively through the Notch ligand Jagged2 expressed by the multipotent HPC subset, as assessed by small interfering RNA (siRNA) silencing. Conversely, notwithstanding their similar multilineage microchimerism, neither sorted Jagged2(-) HPCs nor Jagged2(lo) medullary HSCs were able to expand Treg cells. These data provide evidence for a productive Notch-mediated interaction between a unique subset of mobilized hematopoietic progenitors and Treg cells. They open therapeutic perspectives for autologous transplantation of Jagged2(+) LSK progenitors to promote Treg cell expansion in T cell-mediated diseases.     

复可托治疗小儿反复肺炎支原体感染的疗效及对 免疫功能和肺功能的影响

目的 探讨复可托治疗小儿反复肺炎支原体感染的疗效及对免疫功能和肺功能的影响。方法 选取我院2015年1月~2017年1月收治的88例反复MP感染患儿为研究对象,采用随机数字表法分为两组,各44例。对照组患儿给予常规治疗,观察组在对照组基础上口服复可托,对比两组患儿临床疗效、免疫指标、肺功能指标。结果 观察组总有效率为97.73%,高于对照组的81.82%,差异有统计学意义（P＜0.05）。观察组患儿IgA、IgM、IgG、CD4+、CD8+、CD4+/CD8+等免疫指标优于对照组,差异有统计学意义（P＜0.05）。观察组患儿肺功能指标FVC、FEV1、PEF、FEF25、FEF50、FEF75均优于对照组,差异具有统计学意义（P＜0.05）。结论 复可托治疗小儿反复MP感染临床疗效显著,可有效改善免疫功能和肺功能。     

Immunological parameters and respiratory functions in patients suffering from atopic bronchial asthma after intravenous treatment with salmon calcitonin.

This study reports the effect of salmon calcitonin on airway function and peripheral blood parameters in asthmatic subjects. The premise for the study is that calcitonin is given to asthmatics that require systemic corticosteroids as a way to counter problems with calcium balance and osteoporosis, and that it has an immunosuppressive effect. Salmon calcitonin (100 IU) was administered to 18 patients with atopic bronchial asthma, and the following spirometric parameters were evaluated: forced vital capacity (FVC), forced expiratory volume in the first second (FEV1), peak respiratory flow rate (PEFR) and forced expiratory flow rates at 25%, 50% and 75% of the forced vital capacity (FEF25%, FEF50% and FEF75%). Calcitonin significantly decreased the levels of FVC and FEV1 by 20 min after starting the infusion. The effect of 500 mg aminophylline, used as a reference drug in this study, was much more profound, with a significant increase in all investigated parameters. Also, the effect of salmon calcitonin on some immune parameters (white blood cell count, number of eosinophils, serum levels of immunoglobulins IgG, IgM and IgA, and serum levels of lymphocytes subpopulations CD3, CD4, CD8 and CD19) was determined in another group of 30 patients suffering from atopic bronchial asthma. Calcitonin at a dose of 100 IU/day subcutaneously for 3 days did not alter the immune parameters studied, thus rendering it safe for such and similar treatment schedules in a variety of medical conditions.     

间充质干细胞诱导小鼠CD8α+ CD11b+ jagged2high调节性树突状细胞的方法

目的:研究小鼠骨髓间充质干细胞(BMSCs)体外诱导CD8α+CD11b+jagged2high调节性树突状细胞(DCregs)的方法。方法:应用4种细胞因子体外刺激BALB/c(H-2d)小鼠骨髓有核细胞(BMCs)3 d,流式细胞术(FCM)分选树突状细胞(DCs),与BMSCs共培养10 d,诱导DCregs产生。FCM分析共培养前后DCs的表型、细胞周期及Notch信号通路中Jagged1、Jagged2配体的表达变化。结果:小鼠BMSCs在体外成功诱导新型DCs转变为DCregs,其CD86、CD80、CD40、MHC-II表达均明显下降(P<0.05),而CD205、Jagged1、Jag-ged2表达均明显上升(P<0.05);细胞周期中(G2+S)期细胞增加。结论:MSC可诱导DC细胞向DCregs转化,该MSC-DCregs具有致免疫耐受性表型,增殖能力提高;MSC诱导免疫耐受的机制可能与上调DC的Jagged1和Jagged2基因表达,激活T细胞Notch信号通路相关。