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Single cell data for plasmodium replication in mouse red blood cells

ABSTRACT: Single cell data for plasmodium replication in mouse red blood cells

PROVIDER: PRJEB47569 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR6748060_1.fastq.gz	Fastqsanger.gz
	ERR6748060_2.fastq.gz	Fastqsanger.gz
	ERR6748070_1.fastq.gz	Fastqsanger.gz
	ERR6748070_2.fastq.gz	Fastqsanger.gz
	ERR6748080_1.fastq.gz	Fastqsanger.gz

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Single cell data for plasmodium replication in mouse red blood cells

Project description:Hypoglycemia is a clinical hallmark of severe malaria, the often-lethal outcome of Plasmodium falciparum infection. Yet, the underlying mechanisms driving the pathogenesis of malaria-associated hypoglycemia remain poorly understood. Here we report that labile heme, an alarmin generated as a byproduct of hemolysis during the blood stage of Plasmodium spp. infection, plays a central role in the development of malaria-associated hypoglycemia. Labile heme recapitulated the hypometabolic response to Plasmodium (chabaudi chabaudi; Pcc) infection in mice, including the development of anorexia, transcriptional repression of hepatic glucose production (HGP) and reduction of glycemia, energy expenditure (EE) as well as core body temperature. While this hypometabolic response is protective against immune-mediated liver damage and anemia, when sustained over time it can lead to hypoglycemia and compromise EE as well as thermoregulation. I response, asexual stages of Plasmodium spp. activate a transcriptional program that reduces virulence in favor of sexual commitment and presumably malaria transmission. In conclusion, malaria-associated hypoglycemia represents a trade-off of a hypometabolic defense strategy against Plasmodium infection.

2021-12-31 | E-MTAB-10939 | biostudies-arrayexpress

CD1c+ dendritic cell activation by Plasmodium falciparum-infected red blood cells

Project description:CD1c+ dendritic cell activation by Plasmodium falciparum-infected red blood cells

2017-11-11 | GSE89087 | GEO

RNA-seq of human peripheral blood mononuclear cells exposed to red blood cells infected with Plasmodium falciparum

Project description:Peripheral Blood Mononuclear Cells were isolated from three individuals. Cells from these biological replicates were exposed to Red Blood Cells (male donor age 27) infected with Plasmodium falciparum, uninfected Red Blood Cells, or RPMI prior to stimulation with PAM3CSK4 (10g/mL) for 0, 4, and 12 hours. Total RNA was extracted using the Aurum Total RNA Mini Kit (BioRad). Samples were eluted in nuclease-free water and analyzed for concentration and fragment analysis using an Agilent Fragment Analyzer (Agilent). For each sample, 0.5 g of total RNA was used to prepare RNA-seq libraries using the TruSeq Stranded Total RNA Library Prep Human/Mouse/Rat kit and the TruSeq RNA single indexes Set A (Illumina) according to the manufacturer’s instructions. Samples were sequenced at the Bauer Sequencing Core at Harvard University on a HiSeq 2500 (Illumina), using paired-end 75bp sequencing.

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Global gene expression of the rodent malaria parasites Plasmodium yoelii, Plasmodium berghei and Plasmodium chabaudi blood-stage parasites

Project description:The purpose of this research is to identify and evaluate the global gene expression of the rodent malaria parasites Plasmodium yoelii, Plasmodium berghei and Plasmodium chabaudi blood-stage parasites and specifically compare the blood stage gene expression profiles of samples derived from previous studies on Plasmodium falciparum, Plasmodium vivax and Plasmodium knowlesi

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Profiling Plasmodium falciparum parasites and human red blood cells after treatment with MMV693183

Project description:Compound MMV693183 was added to either Plasmodium falciparum or uninfected red blood cells. The concentrations used were 240 nM, 24 nM, and 2.4 nM. Untreated parasites and red blood cells were also used as controls.

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Circadian Control of the Response of Macrophages to Plasmodium spp.-Infected Red Blood Cells.

Project description:In this study, we sought to determine whether the intensity of the immune response to Plasmodium spp., the parasite causing malaria, depends on time of infection. For this, we considered the known existence of a circadian clock in immune cells which regulates several aspects of the immune response. Experiments were performed using mouse bone marrow-derived macrophages (BMDMs) stimulated ex vivo with red blood cells infected with Plasmodium berghei ANKA (iRBCs) or uninfected RBCs. First, we identified that lysed iRBCs triggered an immune response in macrophages. Then, by stimulating at 4 different circadian time points (16 h, 22 h, 28 h or 34 h post-synchronization of the cells clock), rhythms in reactive oxygen species and cytokines/chemokines were found. Furthermore, the analysis of the macrophage proteome and phosphoproteome revealed global changes according to treatment (iRBC or RBC) and to the circadian time point. In summary, our findings showed that the circadian clock within macrophages determines the magnitude of immune response upon stimulation with iRBCs, along with changes of the cell proteome and phosphoproteome.

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2022-02-17 | PXD027334 | Pride

Single cell gene expression in mouse Hematopoietic cell and Blood after Plasmodium stimulated

Project description:Plasmodium infection induced change in the Bone marrow and Blood cells. Here we addressed whether a prior Plasmodium infection would imapct the cell type and gene expression of Bone marrow and Blood cells by single cell RNA-seq.

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