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

Ai-Yu Gong; Rui Zhou; Guoku Hu; Jun Liu; Sosnowska, Danuta; Drescher, Kristen M.; Haidong Dong; Xian-Ming Chen
January 2010
Journal of Infectious Diseases;1/1/2010, Vol. 201 Issue 1, p160
Academic Journal
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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