Over-expression and localization of a host protein on the membrane of Cryptosporidium parvum infected epithelial cells.
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SUBMITTER: Yang YL
PROVIDER: S-EPMC2752322 | biostudies-literature | 2009 Nov
REPOSITORIES: biostudies-literature
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Over-expression and localization of a host protein on the membrane of Cryptosporidium parvum infected epithelial cells.
Yang Yi-Lin YL Serrano Myrna G MG Sheoran Abhineet S AS Manque Patricio A PA Buck Gregory A GA Widmer Giovanni G
Molecular and biochemical parasitology 20090722 1
The genus Cryptosporidium includes several species of intestinal protozoan parasites which multiply in intestinal epithelial cells. The impact of this infection on the transcriptome of cultured host cells was investigated using DNA microarray hybridizations. The expression of 14 genes found to be consistently up- or down-regulated in infected cell monolayers was validated with RT PCR. Using immunofluorescence we examined the expression of Protease Activated Receptor-2, which is encoded by one of ...[more]
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2018-04-12 | GSE112991 | GEO
Project description:Cryptosporidium parvum is an opportunistic pathogen in AIDS patients. It is an intracellular but extracytoplasmic parasite residing in a host cell-derived parasitophorous vacuole. It is still poorly understood how this parasite interacts with host cells. We observed that expression of the integrin ?2 (ITGA2) gene in host cells was significantly upregulated upon C. parvum infection, and a higher level of ITGA2 protein was present in the parasite infection sites. The infection could be reduced by the treatment of antibodies against ITGA2 and integrin ?1 (ITGB1) subunits, as well as by type I collagen (an integrin ?2?1 ligand). We also generated stable knockdown of ITGA2 gene expression in HCT-8 cells and observed consistent reduction of parasite infection in these knockdown cells. Collectively, our evidence indicates that host cell ITGA2 might be involved in interacting with Cryptosporidium during infection, probably acting as part of the regulatory elements upstream of the reported recruiting and reorganization of F actin at the infection sites.
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