Analysis of gene expression profiles in the liver and spleen of mice infected with Trypanosoma evansi by using a cDNA microarray
Li, S-Q, Reid, S.A., Fung, M-C, Inoue, N. and Lun, Z-R (2009) Analysis of gene expression profiles in the liver and spleen of mice infected with Trypanosoma evansi by using a cDNA microarray. Parasitology Research, 104 (2). pp. 385-397.
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Trypanosoma evansi, the cause of the disease Surra in livestock, is the most widely geographically distributed pathogenic trypanosome occurring in Africa, South and Central America, and Asia, where it causes significant economic loss. Although many studies have described the histopathology induced in the organs of mice infected with T. evansi, few studies have been conducted on gene expression in these organs. Here we used complementary DNA microarray to analyze the gene expression profiles in the liver and spleen of mice infected with T. evansi (STIB 806) at the peak parasitemia (7 days after infection). A total of 14,000 sequences including full length and partial complementary DNAs representing novel, known, and control genes of mouse were analyzed. Results from GeneOntology annotation showed that 158 genes in the liver and 73 genes in the spleen were up-regulated in the infected mice and that 178 genes in the liver and 117 genes in the spleen of infected mice were down-regulated compared with control (non-infected) mice. Most of these genes are metabolism, transport, protein biosynthesis, transcription factors, and nucleic acid binding protein-related genes. The changes of some important genes, such as heat shock protein 70 and proliferating cell nuclear antigen, were confirmed by quantitative reverse transcriptase polymerase chain reaction and immunohistochemistry. TdT-mediated dUTP-digoxigenin nick end labeling analysis results revealed that extensive apoptosis occurred in the liver of infected mice at the peak of parasitemia. Our results provide a comprehensive profile of changes in gene expression in the liver and spleen of mice infected with T. evansi and may be helpful in understanding the pathogenesis of Surra at a molecular level.
|Publication Type:||Journal Article|
|Murdoch Affiliation:||School of Veterinary and Biomedical Sciences|
|Copyright:||© 2008 Springer-Verlag|
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