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Cryptosporidium parvumInduces B7‐H1 Expression in Cholangiocytes by Down‐Regulating MicroRNA‐513
Author(s) -
AiYu Gong,
Rui Zhou,
Guoku Hu,
Jun Liu,
Danuta Sosnowska,
Kristen M. Drescher,
Haidong Dong,
Xianming Chen
Publication year - 2009
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/648589
Subject(s) - cryptosporidium parvum , biology , transfection , microrna , immune system , apoptosis , microbiology and biotechnology , parasite hosting , cell culture , virology , immunology , gene , biochemistry , genetics , world wide web , computer science
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.

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