4.7 Article

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

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JOURNAL OF INFECTIOUS DISEASES
卷 201, 期 1, 页码 160-169

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OXFORD UNIV PRESS INC
DOI: 10.1086/648589

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  1. National Institutes of Health [R01 AI071321]
  2. Nebraska Tobacco Settlement Biomedical Research Program [LB692]
  3. NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI071321] Funding Source: NIH RePORTER

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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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