Understanding bovine trypanosomiasis and trypanotolerance: the promise of functional genomics

Hill, E. W.; O'Gorman, Grace M.; Agaba, Morris; Gibson, John P.; Hanotte, Olivier; Kemp, Stephen J.; Naessens, Jan; Coussens, Paul M.; MacHugh, David E.

doi:10.1016/j.vetimm.2005.02.004

Cited by 54 publications

(29 citation statements)

References 42 publications

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“…This observation is in agreement with other studies, e.g., Leishmania spp. and T. congolense (Chawla and Vishwakarma 2003;Hill et al 2005). Protein kinase C is the enzyme responsible for initiation of normal oxidative mechanisms in macrophages, which plays an important role in the development of protective immunity by activation of various effector cells (Chawla and Vishwakarma 2003).…”

Section: Differentially Expressed Genes Related To Immune and Inflammmentioning

confidence: 99%

Analysis of gene expression profiles in the liver and spleen of mice infected with Trypanosoma evansi by using a cDNA microarray

Reid

Fung

et al. 2008

Parasitol Res

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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.

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Section: Differentially Expressed Genes Related To Immune and Inflammmentioning

confidence: 99%

Analysis of gene expression profiles in the liver and spleen of mice infected with Trypanosoma evansi by using a cDNA microarray

Reid

Fung

et al. 2008

Parasitol Res

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“…Human African trypanosomiasis (HAT also called sleeping sickness) is caused by Trypanosoma brucei rhodesiense and Trypanosoma brucei gambiense. Bovine Trypanosomiasis or 'nagana' is caused by Trypanosoma brucei brucei (Barrett et al, 2003;Chappuis et al, 2005;Hill et al, 2005). In the case of bovine trypanosomiasis, anemia is considered to be the most prominent immunopathological disease-related feature and the major cause of death associated with this disease (d 'Ieteren et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Role of iron homeostasis in trypanosomiasis-associated anemia

et al. 2008

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“…4 A better understanding of trypanotolerance, the ability of some indigenous breeds of cattle and other ruminants to resist sickness despite latent infection, seems to be the most promising approach to disease control. [5][6][7] A mouse model of genetic control of trypanotolerance exists based on A/J as a susceptible strain and C57BL/6 as a tolerant strain. This model is widely accepted and has led to the identification of five major quantitative trait loci (QTL) on mouse chromosomes 1, 5 and 17, associated with survival time.…”

Section: Introductionmentioning

confidence: 99%

Gene expression profiling in a mouse model for African trypanosomiasis

Kierstein¹,

Noyes²,

Naessens³

et al. 2006

Genes Immun

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This study aimed to provide the foundation for an integrative approach to the identification of the mechanisms underlying the response to infection with Trypanosoma congolense, and to identify pathways that have previously been overlooked. We undertook a large-scale gene expression analysis study comparing susceptible A/J and more tolerant C57BL/6 mice. In an initial time course experiment, we monitored the development of parasitaemia and anaemia in every individual. Based on the kinetics of disease progression, we extracted total RNA from liver at days 0, 4, 7, 10 and 17 post infection and performed a microarray analysis. We identified 64 genes that were differentially expressed in the two strains in non-infected animals, of which nine genes remained largely unaffected by the disease. Gene expression profiling at stages of low, peak, clearance and recurrence of parasitaemia suggest that susceptibility is associated with high expression of genes coding for chemokines (e.g. Ccl24, Ccl27 and Cxcl13), complement components (C1q and C3) and interferon receptor alpha (Ifnar1). Additionally, susceptible A/J mice expressed higher levels of some potassium channel genes. In contrast, messenger RNA levels of a few immune response, metabolism and protease genes (e.g. Prss7 and Mmp13) were higher in the tolerant C57BL/6 strain as compared to A/J.

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Understanding bovine trypanosomiasis and trypanotolerance: the promise of functional genomics

Cited by 54 publications

References 42 publications

Analysis of gene expression profiles in the liver and spleen of mice infected with Trypanosoma evansi by using a cDNA microarray

Analysis of gene expression profiles in the liver and spleen of mice infected with Trypanosoma evansi by using a cDNA microarray

Role of iron homeostasis in trypanosomiasis-associated anemia

Gene expression profiling in a mouse model for African trypanosomiasis

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