Mycoplasma pneumoniae capsular polysaccharides inhibit phagocytosis and membrane molecules expression of dendritic cells
10.3969/j.issn.1000-484X.2018.01.003
- VernacularTitle:肺炎支原体荚膜多糖抑制树突状细胞吞噬和膜分子表达
- Author:
Chun-Yan CHEN
1
;
Zi-Ling LIU
;
Lan YU
;
Lie-Song CHEN
;
Yi-Hua ZENG
;
Xiao-Xing YOU
;
Cui-Ming ZHU
Author Information
1. 南华大学病原生物学研究所
- Keywords:
Mycoplasma pneumoniae;
Capsular polysaccharide;
Dendritic cell;
DC-SIGN;
Phagocytosis;
Membrane molecules
- From:
Chinese Journal of Immunology
2018;34(1):15-18,24
- CountryChina
- Language:Chinese
-
Abstract:
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.
