Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Anti-influenza activity of succinate

ABSTRACT: In the present study, we discovered an unexpected interplay between immunometabolism and antiviral immunity. Profiling of human bronchial epithelial BEAS-2B cells was performed using Agilent’s SurePrint G3 human gene expression microarray kit. A single-color design provided two types of comparison: (i) IAV-infected versus mock-infected cells, and (ii) succinate-treated infected cells versus mock-infected cells.

ORGANISM(S): Homo sapiens

SUBMITTER: Ronan Le Goffic

PROVIDER: E-MTAB-10031 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Transcription profiling by array to investigate the response of mice colon samples when infected by a H3N2 influenza virus.

2019-12-01 | E-MTAB-6707 | biostudies-arrayexpress

RNA-seq of mouse colon to investigate how influenza infection leads to intestinal disorders

Project description:To study the impact of influenza infection on gene expression changes in the colon, mice were intra-nasally infected with 30 plaque forming units of the mouse-adapted H3N2 IAV strain Scotland/20/1974. PBS-treated mice served as controls. The colons were collected 7 days post-infection. The 4 samples presented here are \\"pair feed\\" controls of the samples presented in E-MTAB-6707. To provide the pair-fed group with only as much food daily as is consumed by IAV-infected mice, we restricted the food access during the last three days for 15% (day 4), 35% (day 5) and 85% (day 6), respectively (sacrifice at day 7). Mice were anesthetized at day 0. Food was supplied twice a day to pair-fed animals and water was available at all times. The ad libitum (normally nourished) group mice were allowed unrestricted access to food and water. At the sacrifice, paired-fed mice lost ~15% of body mass.

2021-04-21 | E-MTAB-10036 | biostudies-arrayexpress

Interleukin-22 immunotherapy modulates pulmonary gene expression evocative of enhanced tissue barrier and reduces bacterial systemic invasion during severe influenza

Project description:Severe bacterial (pneumococcal) infections are commonly associated with influenza and are significant contributors to the excess morbidity and mortality of influenza. Disruption of lung tissue integrity during influenza participates in bacterial pulmonary colonization and dissemination out of the lungs. Interleukin (IL)-22 has gained considerable interest in anti-inflammatory and anti-infection immunotherapy over the last decade. In the current study, we investigated the effect of exogenous IL-22 delivery on the outcome of bacterial superinfection post-influenza. Our data show that exogenous treatment of influenza-infected mice with recombinant IL-22 reduces bacterial dissemination out of the lungs but is without effect on pulmonary bacterial burden. We describe an IL-22 specific gene signature in the lung tissue of IAV-infected (and naÃ¯ve) mice that might explain the observed effects. Indeed, exogenous IL-22 modulates gene expression profile in a way suggesting a reinforcement of tissue integrity. Our results open the way to alternative approaches for limiting post-influenza bacterial superinfection, particularly systemic bacterial invasion.

2018-05-31 | E-MTAB-6044 | biostudies-arrayexpress

Transcription profiling of human bronchial epithelial cells stabily expressing a dominant negative form of TLR3 after infection with influenza A virus or not infected

Project description:To explore the host responses associated with TLR3 signaling during IAV infection, we used a human bronchial epithelial cell line stably expressing a dominant negative form of TLR3 (pZERO-hTLR3) and examined global impact of TLR3 through an analysis of gene expression changes compared to control cells at 24 h after infection.

2008-06-01 | E-MEXP-1274 | biostudies-arrayexpress

Study of the host response to an influenza virus infection in a mouse model

Project description:Mice were infected intranasally with 1.5x10E5 PFU and total RNA were extracted from mice lungs at day 3. RNA samples were extracted from mice lung infected or not by influenza virus.

2016-10-19 | E-MTAB-4891 | biostudies-arrayexpress

Influenza infection rewires energy metabolism and induces browning features in adipose cells and tissues

Project description:Influenza A viruses cause epidemics and pandemics with damaging health and economic impacts. Alike any obligate intracellular pathogen, IAVs hijack host cell machinery and energetic resources to multiply within, and eventually exit, the host. Increased fatty acid and cholesterol synthesis, as well as increased glucose metabolism have been identified as the major metabolic changes induced by infection. Besides these effects on metabolism, IAV infection also triggers a variety of innate defense mechanisms within the host cell. Although mainly defined as a virus of the respiratory tract, with airway epithelial cells being its prime cellular habitat, complications outside the site of infection have also been reported. However, whether influenza on its own may impact on endocrine tissues and, thereby, lead to metabolic complications, has never been investigated. Here, we compared the response of preadipocytes and adipocytes to IAV infection, in terms of transcriptomic profiles and bioenergetics. The results showed that IAV triggers a browning adipogenesis process, leading to metabolic reprogramming of the adipose tissue resulting in long-lasting alterations of body metabolism. We conclude that the adipose tissue might be an undervalued organ in influenza pathophysiology.

2019-07-20 | E-MTAB-6646 | biostudies-arrayexpress

Inﬂuenza infection rewires energy metabolism and induces browning features in adipose cells and tissues

Project description:C57BL/6 mice were intranasally inoculated with a sublethal dose of H3N2 Influenza A virus (IAV) or with PBS (mock). At 7 days post-infection (7 dpi, corresponding to the peak inflammatory response in the lungs), IAV-infected and non-infected mice were sacrified and inguinal (SCAT) and visceral (i.e. epididymal) white adipose tissues (EWAT), without associated lymph nodes, were collected. Total RNA were extracted from these tissues and genes differential expression was determined using whole genome oligonucleotide microarrays (G4858A, 8x60k chips SurePrint G3 unrestricted GE, Agilent Technologies).

2020-05-16 | E-MTAB-7984 | biostudies-arrayexpress

Analyses of lung early responses to RSV in the neonatal environment reveal key roles for DC and type I IFN in controlling immunopathologic imprinting.

Project description:The gene expression profile of neonatal versus adult lung, 2 days after an RSV or mock infection was analyzed using whole mouse genome agilent microarrays. Total lung RNA were extracted, labeled with Cy3 and hybridized on Agilent G4122F slides. We used 4 biological replicates per condition.

2015-12-21 | E-GEOD-42759 | biostudies-arrayexpress

IBI_Pasteur_IAV_lungs

Project description:Compare transcription in Lungs for IAV infected mice to those from uninfected mice (BALB/c)

2013-06-17 | E-MEXP-3696 | biostudies-arrayexpress

Influenza A virus-triggered succinylation in lung epithelial cells

Project description:Influenza A virus (IAV) is the etiological agent of a highly contagious acute respiratory disease, which causes a considerable socioeconomic burden despite annual vaccination campaigns. Therefore, it is essential to better understand IAV-host cells interaction to help design innovative antiviral therapies. In that regard, recent studies revealed the interplay between metabolic and immune signaling pathways. However, it remains unknown whether IAV alters lung tissues metabolism and what is its potential functional consequence. Using in vitro and in vivo models as well as human respiratory fluids and in-depth metabolomics analysis, we first found that IAV infection alters the glycolysis and mitochondrial oxidative respiration in lung tissues, leading to the accumulation of several immunometabolites in the bronchoalveolar airspaces. We next focused on one mitochondria-derived metabolite, i.e. succinate as its accumulation was found not only in the lungs of IAV-challenged mice but also in the tracheal fluids of IAV-infected patients. Remarkably, we found that succinate exhibits a potent antiviral activity both in vitro and in vivo as it inhibits H1N1 and H3N2 IAV strains and it strongly decreases IAV-triggered inflammatory response. The underlying inhibiting mechanism involves a disruption of IAV replication cycle. Indeed, succinate prevents specifically the nuclear export of the viral nucleoprotein NP, likely due to a specific succinylation at K87 site. Finally, we showed that mice receiving succinate through the intranasal route are more resistant to IAV pneumonia than mock-treated animals. Hence, our study identifies the metabolite succinate as a novel component of the host antiviral arsenal.

2022-03-24 | PXD018419 | 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