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Parasite strain-specific pathogenesis in murine infections with Trypanosoma brucei

ABSTRACT: Different strains of T. brucei induce different degrees of pathology in infected animals, and TREU927-infected mice display greater splenomegaly and anaemia than 247-infected mice. The analysis of differential host gene expression in infected spleens has allowed the identification of which pathways or processes are crucial in determining the progression of disease, for example IL10, LXR/RXR activation and alternative macrophage activation. We used microarray analysis to examine host gene expression between uninfected and infected mice, and between mice infected with the two trypanosome strains.

ORGANISM(S): Mus musculus

PROVIDER: GSE17049 | GEO | 2009/07/11

SECONDARY ACCESSION(S): PRJNA117775

REPOSITORIES: GEO

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Parasite strain-specific pathogenesis in murine infections with Trypanosoma brucei

Project description:Different strains of T. brucei induce different degrees of pathology in infected animals, and TREU927-infected mice display greater splenomegaly and anaemia than 247-infected mice. The analysis of differential host gene expression in infected spleens has allowed the identification of which pathways or processes are crucial in determining the progression of disease, for example IL10, LXR/RXR activation and alternative macrophage activation. We used microarray analysis to examine host gene expression between uninfected and infected mice, and between mice infected with the two trypanosome strains. Mouse spleens were dissected from infected or uninfected mice 10 days post infection, when the differences in pathology criteria (hepatomegaly, red blood cell numbers, reticulocyte percentage, IL10, IFNg and Il12 levels, and splenomegaly) were the greatest. This allowed a three-way comparison, uninfected vs 247-infected, uninfected vs 927-infected, and 247-infected vs 927-infected, allowing us to analyse genes that are differentially expressed between infected and uninfected spleens, but also crucially allows the differentiation between host gene expression with pathogenic (927) and less pathogenic (247) trypanosome strains.

2010-03-03 | E-GEOD-17049 | biostudies-arrayexpress

Transcriptomes of de novo lab-adapted monomorphic Trypanosoma brucei (EATRO 1125) and naturally monomorphic T. evansi and T. equiperdum.

Project description:Here, we produced a series of monomorphic trypanosome stocks, creating snapshots of the transition from pleomorphism to monomorphism, by continuous rapid syringe-passage in mice using a pleomorphic T. brucei. We then compared the transcriptomes of these artificial monomorphic trypanosomes, alongside several naturally monomorphic T. evansi and T. equiperdum strains, with the pleomorphic T. brucei, to analysis the causes of the monomorphism. Trypanosomes grown in mice were harvested at different stage post infection depend on strains (Detailed information was descrided in overall design), and mRNA profile of each sample was generated by deep sequencing, in triplicate.

2022-02-02 | GSE184265 | GEO

Trypanosoma brucei re-run

Project description:Sequencing of progeny from a Trypanosome brucei genetic crosses between T. brucei 247 and T. brucei 927

| PRJEB2011 | ENA

Digital Gene Expression data of a group 1 Trypanosoma brucei gambiense vs a Trypanosoma brucei brucei

Project description:Trypanosoma brucei gambiense is the causative agent of the fatal human disease African sleeping sickness. Using Digital Gene Expression we have compared the transcriptome of a group 1 T.b.gambiense (Eliane) and a T.b.brucei (STIB 247).

2022-08-31 | GSE23885 | GEO

Trypanosoma brucei re-run

Project description:Sequencing of progeny from a Trypanosome brucei genetic crosses between T. brucei 247 and T. b. gambiense 386

| PRJEB2010 | ENA

TbSAP is a novel chromatin protein repressing metacyclic Variant Surface Glycoprotein expression sites in bloodstream form Trypanosoma brucei

Project description:The African trypanosome Trypanosoma brucei is a unicellular eukaryote, which relies on a protective Variant Surface Glycoprotein (VSG) coat for survival in the mammalian host. A single trypanosome has >2000 VSG genes and pseudogenes of which only one is expressed from one of ~15 telomeric bloodstream form expression sites (BESs). Infectious metacyclic trypanosomes present within the tsetse fly vector also express VSG from a separate set of telomeric metacyclic ESs (MESs). All MESs are silenced in bloodstream form T. brucei. As very little is known about how this is mediated, we performed a whole genome RNAi library screen to identify MES repressors. This allowed us to identify a novel SAP domain containing DNA binding protein which we called TbSAP. TbSAP is enriched at the nuclear periphery and binds both MESs and BESs. Knockdown of TbSAP in bloodstream form trypanosomes did not result in cells becoming more ‘metacyclic’-like. Instead, there was extensive global upregulation of transcripts including MES VSGs, VSGs within the silent VSG arrays as well as genes immediately downstream of BES promoters. TbSAP therefore appears to be a novel architectural chromatin protein playing an important role in silencing the extensive VSG repertoire of bloodstream form T. brucei.

2020-11-04 | GSE160713 | GEO

Digital Gene Expression data of two Trypanosoma brucei hybrids (T.b.brucei crossed with T.b.gambiense (group 2))

Project description:Trypanosoma brucei gambiense is the causative agent of the fatal human disease African sleeping sickness. Using Digital Gene Expression we have compared the transcriptome of two T.b.brucei (STIB 247)xT.b.gambiense (STIB386) hybrids.

2022-08-31 | GSE24435 | GEO

Function of Trypanosome brucei RBP10

Project description:Function of Trypanosome brucei RBP10

| PRJEB13058 | ENA

Vector-borne Trypanosoma brucei parasites develop and persist in artificial human skin as skin tissue forms

Project description:Transmission of Trypanosoma brucei by tsetse flies involves the deposition of the infective quiescent metacyclic stage into the mammalian skin at the site of the fly’s bite. In the skin, the metacyclic parasites reactivate and differentiate into proliferative trypanosomes before colonizing the host's blood and tissues. We have generated an advanced human skin equivalent and used tsetse flies to naturally infect the artificial skin with trypanosomes. We have detailed the chronological order of the parasites' development in the skin and found a rapid activation and differentiation of the tsetse-transmitted cell cycle‑arrested metacyclic trypanosomes to proliferative parasites. Single-parasite transcriptomics documented the biological events during differentiation and host invasion at five different time points. After the establishment of a proliferative trypanosome population in the skin, the parasites entered a reversible quiescence program characterized by slow replication and a strongly reduced metabolism. We termed these quiescent trypanosomes skin tissue forms (STF), which may play an important role in maintaining the trypanosome infection in aparasitemic, asymptomatic individuals.

2021-05-30 | GSE174198 | GEO

In vitro generation of human high-density-lipoprotein-resistant Trypanosoma brucei brucei

Project description:The host range of African trypanosomes is influenced by innate protective molecules in the blood of primates. A subfraction of human high-density lipoprotein (HDL) containing apolipoprotein A-I, apolipoprotein L-I, and haptoglobin-related protein is toxic to Trypanosoma brucei brucei but not the human sleeping sickness parasite Trypanosoma brucei rhodesiense. It is thought that T. b. rhodesiense evolved from a T. b. brucei-like ancestor and expresses a defense protein that ablates the antitrypanosomal activity of human HDL. To directly investigate this possibility, we developed an in vitro selection to generate human HDL-resistant T. b. brucei. Here we show that conversion of T. b. brucei from human HDL sensitive to resistant correlates with changes in the expression of the variant surface glycoprotein (VSG) and abolished uptake of the cytotoxic human HDLs. Complete transcriptome analysis of the HDL-susceptible and -resistant trypanosomes confirmed that VSG switching had occurred but failed to reveal the expression of other genes specifically associated with human HDL resistance, including the serum resistance-associated gene (SRA) of T. b. rhodesiense. In addition, we found that while the original active expression site was still utilized, expression of three expression site-associated genes (ESAG) was altered in the HDL-resistant trypanosomes. These findings demonstrate that resistance to human HDLs can be acquired by T. b. brucei. Keywords: Trypanosoma, VSG, antigenic switching, HDL-resistance

2007-07-04 | GSE8369 | GEO

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