Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Inflammatory response of 3D brain microvessels to TNF and Plasmodium falciparum

ABSTRACT: Inflammatory response of 3D brain microvessels to TNF and Plasmodium falciparum

PROVIDER: PRJNA946310 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR23908400_1.fastq.gz	Fastqsanger.gz
	SRR23908400_2.fastq.gz	Fastqsanger.gz
	SRR23908380_1.fastq.gz	Fastqsanger.gz
	SRR23908380_2.fastq.gz	Fastqsanger.gz
	SRR23908381_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 42

Similar Datasets

Inflammatory response of 3D brain microvessels to TNF and Plasmodium falciparum

Project description:Sequestration of Plasmodium falciparum-infected erythrocytes (IEs) in the brain microcirculation is a hallmark of cerebral malaria (CM), leading to endothelial activation, microvascular occlusion, brain swelling, and death. The inflammatory pathogenesis is however poorly understood, partly due to the lack of suitable in vitro platforms to study CM biology. Here, we used 3D perfusable brain microvessels to investigate combinatorial pathogen and host inflammatory stimuli over the in situ parasite maturation and IE rupture. Whereas tumor necros factor (TNF) potently upregulated adhesion molecules and inflammatory pathways, and uniformly recruited leukocytes throughout the microvessels, P. falciparum-IEs upregulated unique stress response pathways, induced minor junctional disturbances and low levels of endothelial apoptosis, and preferentially recruited leukocytes at IE binding regions. Furthermore, parasites delayed recovery from TNF stimulation and enhanced inflammatory responses. Our findings offer insights into CM biology, and suggest that multiple events intersect to promote brain barrier inflammation in CM.

2023-09-30 | GSE227672 | 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.

2022-08-20 | GSE211439 | GEO

Plasmodium falciparum

Project description:Plasmodium falciparum Epigenomics

| PRJNA349753 | ENA

Plasmodium falciparum NF54 Transcriptome

Project description:Transcriptomic Analysis of Cultured Sporozoites of P. falciparum RNA-seq reads from each of three developmental stages (2 replicates per sample) were mapped to the reference Plasmodium falciparum genome, and gene expression levels were calculated for each sample.

2013-12-03 | E-GEOD-52867 | biostudies-arrayexpress

Transcription profiling of human endothelial cells treated with Plasmodium falciparum-infected erythrocytes and/or TNF-alpha

Project description:Sensitisation of endothelium to TNFalpha induced by cytoadherence of Plasmodium falciparum infected red blood cells

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

Plasmodium falciparum

Project description:Plasmodium falciparum malaria studies

| PRJNA447987 | ENA

Plasmodium falciparum

Project description:Transcriptomics of Plasmodium falciparum

| PRJNA447989 | ENA

Plasmodium falciparum

Project description:Plasmodium falciparum Genome sequencing