Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

HERPES SIMPLEX VIRUS TYPE 1 IMPAIRS DENDRITIC CELL FUNCTION BY REMODELLING NEUTRAL LIPID METABOLISM AND INDUCING LIPID DROPLET ACCUMULATION

ABSTRACT: Herpes simplex virus type 1 (HSV-1) infects dendritic cells (DCs), professional antigen-presenting cells that initiate and regulate host antiviral responses. HSV-1 infects DCs limiting their maturation, migration to draining lymph nodes and T cell activation capacity, ultimately promotes their apoptosis. Here, we investigated the impact of HSV-1 infection over neutral lipid metabolism in DCs and their function. We found that HSV-1 significantly alters neutral lipid metabolism in infected DCs and promotes LD accumulation. Pharmacological inhibition of cholesterol ester synthesis, or fatty acid transporter proteins in infected DCs reduced LD accumulation and viral replication, enhanced DC viability and DC migration to draining lymph nodes and promoted DC priming of virus-specific CD8+ T cells. These findings highlight the role of neutral lipid metabolism in HSV-1-infected DCs and its impact over host immunity against this virus, underscoring lipid metabolism in DCs as a potential therapeutical target for triggering antiviral immunity against HSV-1.

INSTRUMENT(S): Liquid Chromatography MS - positive - reverse phase

PROVIDER: MTBLS5163 | MetaboLights | 2025-04-03

REPOSITORIES: MetaboLights

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	10_43_01_14553.abf	Other
	10_43_01_14553.mzML	Mzml
	11_29_01_14539.abf	Other
	11_29_01_14539.mzML	Mzml
	12_47_01_14557.abf	Other

Items per page:

1 - 5 of 154

Similar Datasets

HERPES SIMPLEX VIRUS TYPE 1 IMPAIRS DENDRITIC CELL FUNCTION BY REMODELLING NEUTRAL LIPID METABOLISM AND INDUCING LIPID DROPLET ACCUMULATION

Project description:Herpes simplex virus type 1 (HSV-1) infects dendritic cells (DCs), professional antigen-presenting cells that initiate and regulate host antiviral responses. HSV-1 infects DCs limiting their maturation, migration to draining lymph nodes and T cell activation capacity, ultimately promotes their apoptosis. Here, we investigated the impact of HSV-1 infection over neutral lipid metabolism in DCs and their function. We found that HSV-1 significantly alters neutral lipid metabolism in infected DCs and promotes LD accumulation. Pharmacological inhibition of cholesterol ester synthesis, or fatty acid transporter proteins in infected DCs reduced LD accumulation and viral replication, enhanced DC viability and DC migration to draining lymph nodes and promoted DC priming of virus-specific CD8+ T cells. These findings highlight the role of neutral lipid metabolism in HSV-1-infected DCs and its impact over host immunity against this virus, underscoring lipid metabolism in DCs as a potential therapeutical target for triggering antiviral immunity against HSV-1.

2025-04-08 | GSE238169 | GEO

Rat cytomegalovirus efficiently replicates within dendritic cells and affects both surface marker and gene expression

Project description:Dendritic cells (DC) play a crucial role in generating and maintaining antiviral immunity. While DC are implicated in the antiviral defense by inducing T cell responses, they can also become infected by Cytomegalovirus (CMV). CMV is not only highly species-specific but also specialized in evading immune protection, and this specialization is in part due to characteristic genes encoded by a given virus. Here, we investigated whether RCMV can infect XCR1+ DC and if infection of DC alters the expression of cell surface markers and migration behavior. We demonstrate that wild-type RCMV and a _vxcl1 mutant virus infect splenic rat DC ex vivo and identify viral assembly compartments. Replication-competent RCMV reduced XCR1 and MHCII surface expression. Further, gene expression of infected DC was analyzed by single cell RNA-sequencing. RCMV infection reverted a state of DC activation that was induced by DC cultivation. On the functional level, we observed impaired chemotactic activity of infected XCR1+ DC compared to mock treated cells. We therefore speculate that as a result of RCMV infection, DC exhibit diminished XCR1 expression and are thereby inhibited from the lymphocyte crosstalk.

2023-05-15 | GSE232184 | GEO

Cross-presenting CD103+ dendritic cells are protected from influenza virus infection

Project description:CD8+ cytotoxic T cells are critical for viral clearance from the lungs upon influenza virus infection. The contribution of cross-presentation to the induction of anti-viral cytotoxic T cells remains debated. Here, we used a recombinant influenza virus expressing a NS1-GFP reporter gene to visualize the route of antigen presentation by lung dendritic cells (DC) upon viral infection in vivo. We found that lung CD103+ DC are the only subset to carry intact GFP protein to the draining lymph nodes. Strikingly, lung migratory CD103+ DC are not productively infected by influenza virus and thus induce virus-specific CD8+ T cells through the cross-presentation of antigens from virally infected cells. We also show that CD103+ DC resistance to infection correlates with an increased antiviral state in these cells that is dependent on the expression of IFN receptor alpha. In conclusion, these results establish that efficient cross-priming by migratory lung DC is coupled to the acquisition of an anti-viral status, which is dependent on type I IFN signaling pathway. mRNA profiles were generated by deep-sequencing in Illumina HiSeq2000 from alveolar macrophages and CD103+ dendritic cells from lungs of untreated and flu-treated mice

2013-06-19 | E-GEOD-38838 | biostudies-arrayexpress

Cross-presenting CD103+ dendritic cells are protected from influenza virus infection

2013-06-19 | GSE38838 | GEO

Genome wide analysis of the host antiviral response to dengue virus infection in primary human monocyte-derived dendritic cells

Project description:Analysis of the host response to dengue virus at gene expression level. The hypothesis tested in the present study was that dengue virus triggers and regulate different pathaway with different kinetics controlling the antiviral, the inflammatory and the apoptotic response in primary human DC. Results provide important information of the response to DC to dengue virus showing that antioxidant genes are early stimulated after denv infection reflecting an early production of reactive oxygen species. Interestingely, we demonstrated that ROS production and antiviral and apoptotic responses intersect since chemical inhibition of ROS impairs antiviral and apoptotic responses in these cells. Total RNA obtained from in vitro dengue infected primary human dendritic cells at 0, 6, 12, 18, 24 hours compared to uninfected cells at time 0

2014-12-18 | E-GEOD-58278 | biostudies-arrayexpress

Arabidopsis LDIP is an LDAP-interacting protein that influences lipid droplet biogenesis and neutral lipid homeostasis in both leaves and seeds

Project description:Cytoplasmic lipid droplets (LDs) are found in all types of plant cells where they are derived from the endoplasmic reticulum (ER) and function as a repository for neutral lipids, as well as serving in lipid remodelling and signalling. However, the mechanisms underlying the formation and functioning of plant LDs, particularly in non-seed tissues, are relatively unknown. Previously, we showed that the LD-Associated Proteins (LDAPs) are a family of plant-specific, LD surface-associated coat proteins that are required for proper LD biogenesis and neutral lipid homeostasis in vegetative tissues. Here, we screened a yeast two-hybrid library using Arabidopsis LDAP3 as ‘bait’ in an effort to identify other novel LD protein constituents. One of the candidate LDAP3-interacting proteins was Arabidopsis At5g16550, which is a plant-specific protein of unknown function that we termed LDIP (LDAP-interacting protein). Using a combination of biochemical and cellular approaches, we show that LDIP targets specifically to the LD surface, contains a discrete amphipathic -helical targeting sequence, and participates in both homotypic and heterotypic associations with itself and LDAP3, respectively. Analysis of LDIP T-DNA knockdown and knockout mutants showed a decrease in LD abundance and increase in variability of LD size in leaves, with concomitant increases in total neutral lipid content. Similar phenotypes were observed in plant seeds, which showed enlarged LDs and increases in total seed oil amounts. Collectively, these data identify LDIP as a new player in LD biogenesis in plants that modulates both LD size and cellular neutral lipid homeostasis. Potential mechanisms of LDIP activity are discussed.

2017-11-06 | PXD007192 | Pride

Splenic fibroblastic reticular cells regulate dendritic cell maturation and T-DC interactions required for antiviral immunity

Project description:Stromal cells construct the architecture of the spleen and provide crucial signals that influence the homeostasis and migration of immune cells in the steady state. Fibroblastic Reticular Cells (FRCs) respond to infection via the regulation of many key structural and functional components. Yet, how spleen FRCs contribute to the induction and maintenance of antiviral T cell responses is still poorly defined. We found that ablation of splenic FRCs impacted the generation of virus-specific CD8 T cell during lymphocytic choriomeningitis virus (LCMV) infection in mice. Imaging revealed that during T cell priming in the presence of FRCs, CD8 T cells clustered in the T cell zone with type 1 conventional dendritic cells (cDC1) before moving to the marginal zone to interact with virus-infected cells. In the absence of FRCs, T cells instead clustered with virus-infected cells and cDC1s in the marginal zone, undergoing suboptimal priming due to reduced TCR signalling and unstable DC-T cell interactions. We found that FRCs regulated the early inflammatory wave required for optimal DC activation in vivo. The absence of FRCs thus resulted in diminished DC activation and impaired capacity to prime T cell responses. We further revealed that the presence of an intact FRC network was crucial for the generation of functional effector T cells. Importantly, these early cellular events orchestrated by FRCs also regulated the generation of protective memory T cells upon resolution of infection. Altogether, our study reveals important roles for FRCs for induction of antiviral T cell responses through support for DC maturation, effector CTL generation and the formation of protective memory T cells.

2024-08-16 | GSE274926 | GEO

IRF-3, IRF-5, and IRF-7 coordinately regulate the type I IFN response in myeloid dendritic cells downstream of MAVS signaling

Project description:Myeloid dendritic cells from WT, Irf3-/-xIrf7-/-, Irf3-/-xIrf5-/-xIrf7-/-, Mavs-/- (IPS1-/-)and Ifnar-/- mice were infected with West Nile virus to assess the contributions of specific signaling and transcription factors in initiating the antiviral response RPMI + rmGM-CSF purified bone marrow derived myeloid DC (mDC), mock and WNV infected with insect derived virus and RNA isolated at 24 hours post infection . Each genotype has matched mock and infected samples. n=6 for WT mock, WT infected, IFNAR mock, IFNAR infected, IRF3x7 infected; n=5 IRF3x7 infected; n=3 IRF3x5x7 mock, IRF3x5x7 infected, MAVS mock, MAVS infected. RNA was prepared using the Illumina bead station assay and hybridized to Illumina RefSeq-8 V2 BeadChips. Note: MAVS=IPS1

2013-04-23 | E-GEOD-41355 | biostudies-arrayexpress

Transcriptomics of vitamin D treatment effects in Mycobacterium tuberculosis-infected THP-1 cells

Project description:Previous reports have shown low vitamin D serum levels and polymorphisms in the vitamin D receptor (VDR) to be associated with increased risk for TB. Given that 1α,25-dihydroxyvitamin D3 has a role in lipid metabolism control, we tested whether the link between 1α,25-dihydroxyvitamin D3 and tuberculosis involves macrophage lipid metabolism. Since formation of lipid droplets (LD) is a hallmark of lipid dysregulation in M. tuberculosis-infected macrophages, we measured LD content as a readout of altered lipid metabolism in infected THP-1 cells. Induction of LD, which peaked by 24 hours post-infection was prevented by addition of 1α,25-dihydroxyvitamin D3 at the time of infection. To investigate the mechanism of 1α,25-dihydroxyvitamin D3 modulation of LD formation, we analyzed the transcriptome of M. tuberculosis-infected THP-1 cells with and without 1α,25-dihydroxyvitamin D3 treatment.

2014-07-01 | GSE57028 | GEO

Quantitative Lipid Droplet Proteome Analysis Identifies Annexin A3 as a Cofactor for HCV Particle Production

Project description:Cytosolic lipid droplets (LDs) are vital to Hepatitis C Virus (HCV) infection as the putative sites of virion assembly. To identify novel regulators of HCV particle production, we performed quantitative LD proteome analysis. Huh7.5 cells were labeled by stable isotope labeling with heavy amino acids in cell culture (SILAC) and subsequently infected with an HCV Jc1 reporter virus. After selection for HCV-infected cells, equal amounts of HCV-infected and uninfected control cells were mixed, LDs were isolated and analyzed by LC-ESI-MS/MS.

2016-09-26 | PXD004707 | Pride

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