Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Plasmodium Infection induces gene expression changes in spleen lymphocytes

ABSTRACT: Plasmodium infection induced trained immunity in mice. As splenomegaly is obvious upon Plasmodium infection, we aim to determine whether the the protective effect of plasmodium-induced trained immunity is due to the effector function induced by splenomegaly.

ORGANISM(S): Mus musculus

PROVIDER: GSE198699 | GEO | 2022/11/11

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Plasmodium Infection induces gene expression changes in spleen lymphocytes

Project description:Plasmodium Infection induces gene expression changes in spleen lymphocytes

| PRJNA816497 | ENA

Transcriptome and Epigenome Characterization of Long Term Trained Immunity in Cotrolled Human Malaria Model [RNA-seq]

Project description:Innate immune memory responses (also termed ‘trained immunity’) have been described in monocytes after BCG vaccination and after stimulation in vitro with microbial and endogenous ligands such as muramyl dipeptide, β-glucan, oxidized LDL, and MSU crystals. Whether clinical infections are also capable of inducing a trained immunity phenotype has not been studied. We evaluated whether Plasmodium falciparum infection can induce innate immune memory by assessing monocyte epigenetic, transcriptional and functional (cytokine production) programs from five volunteers undergoing controlled human malaria infection. During acute infection monocytes produced lower amounts of inflammatory cytokines upon secondary stimulation, but 36 days after malaria infection they produced significantly higher IL-6 and TNF-α in response to various stimuli. Furthermore, transcriptomic and epigenomic data analysis revealed a clear reprogramming of monocytes after malaria infection. Plasmodium challenge induces a long-term deposition of H3K4me3 at the promoter regions of several inflammatory genes of monocytes, these changes remaining stable for several weeks after infection. These findings demonstrate an epigenetic basis of trained immunity in the model of controlled in vivo human malaria infection.

2020-12-21 | GSE137043 | GEO

Transcriptome and Epigenome Characterization of Long Term Trained Immunity in Cotrolled Human Malaria Model [ChIP-seq]

2020-12-21 | GSE137042 | GEO

Epigenetic regulation of gene expression in mouse Hematopoietic cell after Plasmodium stimulated

Project description:Plasmodium infection induced change in the hematopoietic stem cell (HSC) compartment. Here we addressed whether a prior Plasmodium infection would imapct the epignetic profile of HSCs by ATAC-seq.

2022-11-11 | GSE198603 | GEO

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.

2024-07-01 | GSE240202 | GEO

Whole spleen transcriptome during acute phase of infection in an avirulent Plasmodium chabaudi chabaudi AS infection.

Project description:The spleen is considered as the major lymphoid organ involved in generating immune responses to the erythrocytic stages of the malaria parasite, Plasmodium, but access to human spleens is not practical and most studies rely on peripheral blood for assessing immune responses. However, the suitability of peripheral blood as a proxy for splenic immune responses is unknown. Here, we have analysed transcriptome activity for whole spleens over 12 days of erythrocytic stage Plasmodium chabaudi infection in C57BL/6 mice. These data will be compared with comparable data taken from whole blood: and previously published: GSE93631

2019-11-19 | GSE123391 | GEO

Innate Immune Training of Human Macrophages by Cathelicidin Analogs

Project description:Trained innate immunity can be induced in human macrophages by microbial ligands, but it is unknown if exposure to endogenous alarmins such as cathelicidins can have similar effects. Previously, we demonstrated sustained protection against infection by the chicken cathelicidin-2 analog DCATH-2. Thus, we assessed the capacity of cathelicidins to induce trained immunity. PMA23 differentiated THP-1 (dTHP1) cells were trained with cathelicidin analogs for 24 hours, and restimulated after a 3-day rest period. DCATH-2 training of dTHP-1 cells amplified their proinflammatory cytokine response when restimulated with TLR2/4 agonists. Trained cells displayed a biased cellular metabolism towards mTOR-dependent aerobic glycolysis and long-chain fatty acid accumulation and augmented microbicidal activity. DCATH-2-induced trained immunity was inhibited by histone acetylase inhibitors, suggesting epigenetic regulation, and depended on caveolae/lipid raft-mediated uptake, MAPK p38 and purinergic signaling. To our knowledge, this is the first report of trained immunity by host defense peptides.

2022-07-11 | MTBLS4495 | MetaboLights

scRNA-seq of mouse Plasmodium-specific TCR-transgenic CD4+ T cells prior to and after re-infection.

Project description:Naturally-acquired immunity to blood-stage malaria is associated with several effector CD4 + T subsets including germinal centre (GC) Tfh, Th1 and Tr1 cells. Children in malaria-endemic regions can experience repeated Plasmodium infections over short periods of time; yet the effect of reinfection on multiple co-existing effector and memory subsets remains unclear. Here, we tracked antigen-experienced TCR-transgenic CD4+ T cells during Plasmodium re-infection in mice using scRNA-seq.

2024-05-02 | GSE233703 | GEO

Time series of Balb/c spleen infected with Plasmodium yoelii non-lethal vs lethal strains

Project description:Knowledge on the dynamic features of the processes driven by malaria parasites in the spleen, our biggest lymphoid organ, is lacking. We have implemented intravital microscopy and magnetic resonance imaging of the mouse spleen in experimental infections with the Plasmodium yoelii non-lethal (17X) and lethal (17XL) strains. Notably, there was higher parasite accumulation, reduced motility, lost of directionality and different T2 relaxation times only in spleens of mice infected with the 17X strain. Moreover, these differences were associated with the formation of a strain-specific induced spleen tissue barrier, with macrophage-clearance escape, and with cytoadherence of infected reticulocytes to this barrier. This is a novel spleen-immune evasion mechanism in which parasite-induced spleen remodeling and adherence to this organ allow establishment of chronic infections. We performed time-series global transcriptional analyses from spleens of mice infected with the P. yoelii 17X and 17XL strains at days 3, 4, 5, 10% and 50% of parasitemia post-infection, together with non-infected spleens as a reference day 0, using commercially available arrays representing the complete mouse genome (Agilent Whole Mouse Genome G4122A).

2010-10-12 | E-GEOD-17603 | biostudies-arrayexpress

Anopheles gambiae immune responses to human and rodent Plasmodium parasite species

Project description:Transmission of malaria is dependent on the successful completion of the Plasmodium lifecycle in the Anopheles vector. Major obstacles are encountered in the midgut tissue, where most parasites are killed by the mosquito’s immune system. In the present study, DNA microarray analyses have been used to compare Anopheles gambiae responses to invasion of the midgut epithelium by the ookinete stage of the human pathogen Plasmodium falciparum and the rodent experimental model pathogen P. berghei. Invasion by P. berghei had a more profound impact on the mosquito transcriptome, including a variety of functional gene classes, while P. falciparum elicited a broader immune response at the gene transcript level. Ingestion of human malaria-infected blood lacking invasive ookinetes also induced a variety of immune genes, including several anti-Plasmodium factors. Keywords: Anopheles gambiae, Plasmodium falciparum, ookinete, invasion, innate immunity

2007-08-15 | GSE8789 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data