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Vet Res. 2010 Sep-Oct;41(5):70. doi: 10.1051/vetres/2010041. Epub 2010 Jul 12.

Microarray-based transcriptional profiling of Eimeria bovis-infected bovine endothelial host cells.

Author information

1
Institute of Parasitology, Justus Liebig University Giessen, Rudolf-Buchheim-Str. 2, 35392 Giessen, Germany. anja.taubert@vetmed.uni-giessen.de

Abstract

Within its life cycle Eimeria bovis undergoes a long lasting intracellular development into large macromeronts in endothelial cells. Since little is known about the molecular basis of E. bovis-triggered host cell regulation we applied a microarray-based approach to define transcript variation in bovine endothelial cells early after sporozoite invasion (4 h post inoculation (p.i.)), during trophozoite establishment (4 days p.i.), during early parasite proliferation (8 days p.i.) and towards macromeront maturation (14 days p.i.). E. bovis infection led to significant changes in the abundance of many host cell gene transcripts. As infection progressed, the number of regulated genes increased such that 12, 45, 175 and 1184 sequences were modulated at 4 h, 4, 8 and 14 days p.i., respectively. These genes significantly interfered with several host cell functions, networks and canonical pathways, especially those involved in cellular development, cell cycle, cell death, immune response and metabolism. The correlation between stage of infection and the number of regulated genes involved in different aspects of metabolism suggest parasite-derived exploitation of host cell nutrients. The modulation of genes involved in cell cycle arrest and host cell apoptosis corresponds to morphological in vitro findings and underline the importance of these aspects for parasite survival. Nevertheless, the increasing numbers of modulated transcripts associated with immune responses also demonstrate the defensive capacity of the endothelial host cell. Overall, this work reveals a panel of novel candidate genes involved in E. bovis-triggered host cell modulation, providing a valuable tool for future work on this topic.

PMID:
20615380
PMCID:
PMC2920636
DOI:
10.1051/vetres/2010041
[Indexed for MEDLINE]
Free PMC Article

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