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Differentially expressed genes upon melatonin treatment on Plasmodium falciparum infected red blood cells

ABSTRACT: Differentially expressed genes upon melatonin treatment on Plasmodium falciparum infected red blood cells

PROVIDER: PRJEB9674 | ENA |

REPOSITORIES: ENA

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Differentially expressed genes upon melatonin treatment on Plasmodium falciparum infected red blood cells

Project description:To investigate, by RNA-Sequencing (RNA-seq), the expression profile of two P. falciparum strains (control 3D7; protein kinase 7 knock-out strain, Pfpk7- and PfpK7 complement) to the presence of melatonin.

2016-10-01 | E-MTAB-3667 | 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

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2007-06-05 | E-SGRP-3 | biostudies-arrayexpress

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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Genome-wide analysis of transcription factor PfNF-YB in Plasmodium falciparum.

Project description:PfNF-YB is a transcription factor of Plasmodium falciparum and is known as a CCAAT-box-binding subunit B. PfNF-YB belongs to NF-Y complex family that is conserved from yeast to human. PfNF-YB is highly expressed in schizont stage and co-localized at the nucleus in mature form during intraerythrocytic stage. We found that melatonin and cAMP second messenger can modulate the PfNF-YB expression in P. falciparum. To better understand the function of PfNF-YB in P. falciparum we proposed to perform chromatin immunoprecipitation (ChIP) of PfNF-YB together with chromatin profiling by ChIP-on-chip analysis. The results showed that PfNF-YB binds to CCAAT of several genes in schizont stage.

2013-07-16 | GSE48894 | GEO

Plasmodium falciparum and TNF-a Differentially Regulate Inflammatory and Barrier Integrity Pathways in Human Brain Endothelial Cells

Project description:Cerebral malaria is a severe complication of Plasmodium falciparum infection characterized by the loss of blood-brain barrier (BBB) integrity, which is associated with brain swelling and mortality in patients. P. falciparum-infected red blood cells and in!ammatory cytokines, like tumor necrosis factor alpha (TNF-a), have been implicated in the development of cerebral malaria, but it is still unclear how they contribute to the loss of BBB integrity. Here, a combination of transcriptomic analysis and cellular assays detecting changes in barrier integrity and endothelial activation were used to distinguish between the effects of P. falciparum and TNF-a on a human brain microvascular endothelial cell (HBMEC) line and in primary human brain microvascular endothelial cells. We observed that while TNF-a induced high levels of endothelial activation, it only caused a small increase in HBMEC permeability. Conversely, P. falciparum-infected red blood cells (iRBCLs) led to a strong increase in HBMEC permeability that was not mediated by cell death. Distinct transcriptomic pro"les of TNF-a and P. falciparum in HBMECs con"rm the differential effects of these stimuli, with the parasite preferentially inducing an endoplasmic reticulum stress response. Our results establish that there are fundamental differences in the responses induced by TNF-a and P. falciparum on brain endothelial cells and suggest that parasite-induced signaling is a major component driving the disruption of the BBB during cerebral malaria, proposing a potential target for much needed therapeutics.

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Project description:To explore the detailed mechanism by which melatonin allivates TNF-α induced HCAECs damage, we performed RNA-seq in control and melatonin treated HCAECs, and identified 213 upregualted and 103 downregulated genes with the criterion of |FC|≥2 and p≤0.05.

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Exvivo Experiment

Project description:Healthy Kenyan children with (n=10) or without (n=14) a previous history of complicated Plasmodium falciparum infection had aliquots of their whole-blood cultured ex-vivo and either mock infected or infected with Plasmodium falciparum (A4 strain) for 5 (n=24) and 9 hours (n=11). A clinical history design type is where the organisms clinical history of diagnosis, treatments, e.g. vaccinations, surgery etc. Time: lenght of co-culture Infection: whole-blood cells cultured ex-vivo in the presence of either uninfected red blood cells or red blood cells infected with Plasmodium falciparum Disease State: Healthy individuals with (PrevHxMal) or without (NoHxMal) previous exposure to complicated Plasmodium falciparum infection

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Expression data of gene knockout Plasmodium falciparum clones

Project description:The variant antigen, Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1), expressed on the surface of P. falciparum infected Red Blood Cells (iRBCs) is a critical virulence factor for malaria. Each parasite encodes 60 antigenically distinct var genes encoding PfEMP1s, but during infection the clonal parasite population expresses only one gene at a time before switching to the expression of a new variant antigen as an immune evasion mechanism to avoid the hostM-bM-^@M-^Ys antibody responses. The mechanism by which 59 of the 60 var genes are silenced remains largely unknown. We used microarrays to detail the global programme changes of gene expression caused by each gene knockout with a particular view towards which gene knockout results in transcriptional upregulation of the entire var gene family. Plasmodium falciparum clones, in each of which one of different histone lysine methylation modification enzyme genes was knocked out, were synchronized in the asexual stage and collected at indicated time points post invasion of erythrocytes for RNA extraction and hybridization on Affymetrix microarrays. We sought to identify the key epigenetic enzyme that controls silencing of the whole var gene family.

2013-05-25 | E-GEOD-47349 | biostudies-arrayexpress

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