目的探讨地塞米松对哮喘小鼠CD4^+、CD25^+调节性T细胞(regulatory T cells,Treg)及IL-4、TGF-β水平的影响。方法 30只雄性BALB/c小鼠随机分为正常对照组、哮喘组及地塞米松组3组各10只;利用鸡卵白蛋白腹腔注射、雾化吸入制备哮喘模型;使用流式细胞仪分别检测各组小鼠脾脏单个核细胞CD4^+、CD25^+Treg细胞占CD4^+T细胞的百分比;使用Western Blot方法分析IL-4在小鼠肺组织中的表达情况;使用酶联免疫吸附试验方法检测各组小鼠血清中TGF-β的水平。结果哮喘组小鼠脾单个核细胞CD4^+、CD25^+Treg细胞百分比及TGF-β水平较正常对照组降低(均P<0.05),哮喘组IL-4水平较正常对照组增高(P<0.05),地塞米松组与正常对照组比较,差异无统计学意义(P>0.05)。结论哮喘小鼠CD4^+、CD25^+Treg数量的减少,功能的下降,可能参与了哮喘的发病过程,地塞米松可能通过上调CD4^+、CD25^+Treg比例,调节T细胞亚群失衡来发挥抗炎作用。
Primary pulmonary rhabdomyosarcoma (RMS)is one of the most common soft-tissue malignancies in children, but is rare in persons aged >45 years (Triche,1997; Ferrari et al., 2003). RMS is considered to result from the malignant transformation of primitive mesenchymal cells.
目的探讨哮喘小鼠CD4+CD25+调节性T细胞(regulatory T cells,Treg)及IL-10、TGF-β、IL-17水平的变化。方法 30只雄性BALB/c小鼠被随机分为三组:正常对照组、哮喘组及地塞米松组各10只;利用鸡卵白蛋白腹腔注射、雾化吸入制备哮喘模型;取小鼠左肺组织作病理切片观察炎症改变;通过流式细胞仪检测各组小鼠脾脏单个核细胞CD4+CD25+Treg细胞占CD4+T细胞的百分比;采用酶联免疫吸附试验检测各组小鼠血清中细胞因子IL-1、TGF-β、IL-17表达水平。结果哮喘组小鼠的脾单个核细胞CD4+CD25+Treg细胞百分比以及IL-10、TGF-β的表达水平较正常对照组降低(P<0.05),哮喘组IL-17的表达水平较正常对照组增高(P<0.05),地塞米松组与正常对照组比较,差异无统计学意义(P>0.05)。结论哮喘小鼠体内CD4+CD25+Treg数量的减少以及功能的下降、细胞因子IL-17表达的增加均参与了哮喘的发病过程。
Sialic acid-binding immunoglobulin-like lectin (Siglec)-F is a mouse functional paralog of human Siglec-8 that induces apoptosis in human eosinophils, and therefore may be useful as the basis of treatments for a variety of disorders associated with eosinophil hyperactivity, such as asthma. The expression pattern and functions of this protein in various cell types remain to be elucidated. The aim of this study was to determine the expression of Siglec-F on mouse macrophages by immunocytochemical staining, and also to investigate the effects of Siglec-F engagement by a Siglec-F antibody on phagocytic activity of macrophages. The results showed that Siglec-F expression was detected on mouse alveolar macrophages, but not on peritoneal macrophages. Furthermore, Siglec-F engagement did not affect the phagocytic activity of alveolar macrophages in the resting state or in the activated state following stimulation by the proinflammatory mediator tumor necrosis factor alpha (TNF-α) or lipopolysaccharide (LPS). Siglec-F expression on alveolar macrophages may be a result of adaptation. Macrophages actively regulate immune responses via production of cytokines. Therefore, further investigation of the effects of Siglec-F engagement on immune mediators or cytokines released by alveolar macrophages is required.
