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RNA-Seq of adipose tissue from mice infected with Trypanosoma brucei

ABSTRACT: RNA-Seq of adipose tissue from mice infected with Trypanosoma brucei

PROVIDER: PRJEB30758 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR3048432.fastq.gz	Fastqsanger.gz
	ERR3048433.fastq.gz	Fastqsanger.gz
	ERR3048434.fastq.gz	Fastqsanger.gz
	ERR3048435_1.fastq.gz	Fastqsanger.gz
	ERR3048435_2.fastq.gz	Fastqsanger.gz

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RNA-Seq of adipose tissue from mice infected with Trypanosoma brucei

Project description:The goal of this experiment was to study the alterations that occur in the adipose tissue of mice during a T. brucei infection. Gonadal adipose tissue from C57BL/6J mice infected with T. brucei AnTat 1.1E 90-13 parasites was collected at day 0 and 26 post-infection. Total RNA was extracted from 3 samples of non-infected adipose tissue and 2 samples of adipose tissue on day 26 post-infection. Day 6 post-infection adipose tissue samples (n=3) were already published (E-MTAB-4061).

2019-12-12 | E-MTAB-7596 | biostudies-arrayexpress

IL-17 signalling is critical for controlling subcutaneous adipose tissue wasting and parasite burden during chronic Trypanosoma brucei infection [bulk RNA-seq]

Project description:In the skin, Trypanosoma brucei colonises the subcutaneous white adipose tissue (WAT) and harbours a pool of parasites competent for forward transmission. The interaction between parasites, adipose tissue, and the local immune system is likely to drive adipose tissue wasting and weight loss observed in cattle and humans infected with T. brucei. However, mechanistically, this process is not fully understood. Here, using several complementary approaches including mass cytometry by time of flight, bulk and single cell transcriptomics, we found that T. brucei infection drives a local expansion of several IL-17A-producing cells in the murine WAT, including TH17 and V6+ T cells. We also found that global IL-17 deficiency, or mice lacking IL-17 receptor expression specifically on adipocytes, were protected from infection-induced WAT wasting and weight loss. Unexpectedly, we found that abrogation of IL-17 signalling on adipocytes results in higher burden of extravascular parasites in the WAT. Taken together, our study highlights the central role of IL-17 signalling on adipocytes in controlling WAT responses to infection, suggesting that adipocytes are a critical coordinator of the tissue immune response to T. brucei infection.

2023-05-27 | GSE233311 | GEO

RNA-seq of blood and adipose tissue from mice infected with Trypanosoma brucei

Project description:RNA-seq of blood and adipose tissue from mice infected with Trypanosoma brucei

| PRJEB11801 | ENA

RNA-seq of blood and adipose tissue from mice infected with Trypanosoma brucei

Project description:We asked whether the in-vivo transcriptome of T. brucei AnTat 1.1E 90-13 parasites collected from adipose tissue and blood is different. We collected gonadal adipose tissue of infected mice on day 6 post-infection, when a high number of parasites is expected, and blood on day 4 post-infection when slender-forms are the most abundant form of the parasite. Parasites from blood were purified over a DEAE column. Total RNA was extracted from two independent samples of blood and three independent samples of fat and subjected to RNA-sequencing.

2016-05-26 | E-MTAB-4061 | biostudies-arrayexpress

IL-17 signalling is critical for controlling subcutaneous adipose tissue wasting and parasite burden during chronic Trypanosoma brucei infection [single-cell RNA-seq]

2023-05-27 | GSE233312 | GEO

Trypanosoma brucei brucei

Project description:Trypanosoma brucei brucei VSG-seq

| PRJNA270648 | 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 brucei

Project description:Trypanosoma brucei brucei Raw sequence reads

| PRJNA292451 | ENA

Trypanosoma brucei brucei

Project description:Trypanosoma brucei brucei edited mRNA transcriptomes

| PRJNA369536 | ENA

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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