Cryptosporidium parvum Induces B7-H1 Expression in Cholangiocytes by Down-Regulating MicroRNA-513

被引:57
作者
Gong, Ai-Yu [1 ]
Zhou, Rui [1 ]
Hu, Guoku [1 ]
Liu, Jun [1 ]
Sosnowska, Danuta [1 ]
Drescher, Kristen M. [1 ]
Dong, Haidong [2 ,3 ]
Chen, Xian-Ming [1 ]
机构
[1] Creighton Univ, Med Ctr, Dept Med Microbiol & Immunol, Omaha, NE 68178 USA
[2] Mayo Clin, Dept Urol, Coll Med, Rochester, MN USA
[3] Mayo Clin, Dept Immunol, Coll Med, Rochester, MN USA
基金
美国国家卫生研究院;
关键词
LIGAND-DEPENDENT MECHANISM; EPITHELIAL-CELLS; T-CELLS; BILIARY EPITHELIA; INNATE IMMUNITY; IN-VITRO; INFECTION; APOPTOSIS; RESPONSES; ACTIVATION;
D O I
10.1086/648589
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Expression of B7 costimulatory molecules represents an important compartment of immune response of epithelial cells after microbial infection. We report here that the protozoan parasite Cryptosporidium parvum induced B7-H1 expression in cultured human cholangiocytes. Induced expression of B7-H1 was identified in cells after exposure to infective C. parvum parasite or parasite lysate. Interestingly, the level of microRNA-513 (miR-513) was reduced in cells after exposure to C. parvum, which resulted in a relief of 3' untranslated region-mediated translational suppression of B7-H1. Overexpression of miR-513 through transfection of miR-513 precursor inhibited C. parvum-induced B7-H1 protein expression. Moreover, enhanced apoptotic cell death was identified in activated human T cells after coculture with C. parvum-infected cholangiocytes. The apoptosis of activated T cells was partially blocked by a neutralizing antibody to B7-H1 or transfection of cholangiocytes with miR-513 precursor. These data suggest a role of miR-513 in regulating B7-H1 expression by cholangiocytes in response to C. parvum infection.
引用
收藏
页码:160 / 169
页数:10
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