Project description:Cryptosporidium infects enterocytes, but their contribution to parasite control is not well understood. Early resistance to Cryptosporidium is dependent on the production of IFN gamma. Loss of STAT1 in enterocytes, but not dendritic cells or macrophages, antagonized early parasite control. Moreover, transcriptional profiling of enterocytes from infected mice revealed the induction of an IFN gamma signature that included multiple genes (IDO, GBP, IRG) associated with control of intracellular pathogens.
Project description:Cryptosporidium parvum is an important zoonotic parasitic disease worldwide, but the molecular mechanisms of the host–parasite interaction are not fully understood. Noncoding microRNAs (miRNAs) are considered key regulators of parasitic diseases. Therefore, we used microarray, qPCR, and bioinformatic analyses to investigate the intestinal epithelial miRNA expression profile after Cryptosporidium parvum infection.Twenty miRNAs were differentially expressed after infection (four upregulated and 16 downregulated). Further analysis of the differentially expressed miRNAs revealed that many important cellular responses were triggered by Cryptosporidium parvum infection, including cell apoptosis and the inflammatory and immune responses.This study demonstrates for the first time that the miRNA expression profile of human intestinal epithelium cells is altered by C. parvum infection. This dysregulation of miRNA expression may contribute to the regulation of host biological processes in response to C. parvum infection, including cell apoptosis and the immune responses. These results provide new insight into the regulatory mechanisms of host miRNAs during cryptosporidiosis, which may offer potential targets for future C. parvum control strategies.
