肺炎支原体荚膜多糖抑制树突状细胞吞噬和膜分子表达

目的:了解肺炎支原体(Mp)荚膜多糖(CPS)通过结合树突状细胞特异性细胞间黏附分子-3-结合非整合素分子(DC-SIGN)对树突状细胞吞噬功能及细胞表面膜分子表达的影响。方法:复苏培养Mp 菌株,抽提和纯化CPS。培养人外周血单个核细胞来源的DC,吉姆萨染色观察和流式细胞术(FCM)鉴定;用CPS 刺激DC,FCM 检测DC 对FITC-多聚糖的吞噬指数、DC 表面特异标志CD83、HLA-DR 抗原以及协同刺激分子CD80 和CD86 的表达。结果:培养7 d 的DC 有典型的树突状结构,并高表达CD11c 分子。经CPS 刺激后,DC 内FITC-多聚糖的平均荧光强度较对照PBS 处理组显著增加(P<0.05),DC 表面膜分子CD83、HLA-DR、CD80 和CD86 较对照组显著减少(P<0.05)。用CPS 刺激被DC-SING 受体封闭的DC,发现DC 内FITC-多聚糖吞噬指数和四种膜表面分子的表达与对照组差异均无显著性(P>0.05)。结论:Mp CPS 可促进DC 的吞噬功能和减少细胞膜分子CD83、HLA-DR、CD80 和CD86 的表达。

Mycoplasma pneumoniae capsular polysaccharides inhibit phagocytosis and membrane molecules expression of dendritic cells

Objective:To study the influences of Mycoplasma penumoniae capsular polysaccharide(CPS)on the phagocytosis and membrane molecules expression of the human peripheral blood mononuclear cells derived dendritic cells by binding to dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin(DC-SIGN),so as to know the effect of CPS on the maturation of dendritic cells.Methods: M.pneumoniae strain was cultivated and CPS was extracted.Human peripheral blood mononuclear cells were separated and induced to dendritic cells,then identified the cells by flow cytometry and observation under the microscope.CPS was used to treat dendritic cells or cells pretreated with DC-SIGN monoclonal antibody,and then FITC-dextran phagocytosis and surface markers CD83,HLA-DR,CD80 and CD86 were detected by flow cytometry.Results: The dendritic cells tended to form colony groups.The positive rate of CD11c molecule in the cultured dendritic cells was about 86.27% .After stimulated by CPS, the FITC-dextran fluorescence mean intake by dendritic cells were increased(P<0.05),while the cell surface membrane molecules CD83,HLA-DR,CD80 and CD86 were decreased significantly when compared with the PBS treated control cells(P<0.05).When blocked DC-SIGN with the monoclonal antibody,the FITC-dextran fluorescence mean and membrane molecules expression had no statistical difference with the control cells(P>0.05).Conclusion: M.pneumoniae CPS can promote the phagocytic function of DC and inhibit the expression of CD83,HLA-DR,CD80 and CD86.