Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Streptococcus pneumoniae infection and murine hearat proteome

ABSTRACT: For the last two decades, the three most common causes of death world-wide have been ischemic heart disease, cerebrovascular disease and respiratory tract infections; the latter being caused mainly by the influenza virus and the bacterial pathogen Streptococcus pneumoniae (Spn). Reports through this period of time have shown that elderly patients admitted to the hospital for severe community-acquired pneumonia (CAP), experience ~10-25% mortality rates and up to 40% of them expired within one year. A key contributing factor for the observed high mortality rate are the major adverse cardiac events (MACE) that occur during hospitalization and convalescence9. Notably, during severe pneumococcal infections, Spn, the most common cause of CAP, has been shown to be capable of myocardial invasion, induction of cardiomyocyte death, and disruption of cardiac contractility. In addition, changes to heart functionality have also been reported after influenza infection in humans, however the mechanisms for this remain unclear.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Streptococcus Pneumoniae Tigr4 Mus Musculus (mouse)

TISSUE(S): Heart

SUBMITTER: Yanbao Yu

LAB HEAD: Yanbao Yu

PROVIDER: PXD016137 | Pride | 2021-12-23

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	1DLC031819QE_GJN_KOheart_Flu_BR1_STrap1.raw	Raw
	1DLC031819QE_GJN_KOheart_Flu_BR1_STrap2.raw	Raw
	1DLC031819QE_GJN_KOheart_SpnFlu_BR1_STrap1.raw	Raw
	1DLC031819QE_GJN_KOheart_SpnFlu_BR1_STrap2.raw	Raw
	1DLC031819QE_GJN_KOheart_Spn_BR1_STrap1.raw	Raw

Items per page:

1 - 5 of 69

Similar Datasets

Influenza virus infection leads to global cardiac proteome remodeling during convalescence

Project description:Influenza virus infection leads to global cardiac proteome remodeling during convalescence MTD project_description "Influenza virus infections lead to more than 500,000 hospitalizations in the U.S. every year. Patients with cardiovascular diseases have been shown to be at high risk of influenza mediated cardiac complications. Importantly, recent reports have provided clinical data supporting a direct link between laboratory-confirmed influenza virus infection and adverse cardiac events. However, the molecular mechanisms of how influenza virus infection induces detrimental cardiac changes, even after resolution of the pulmonary infection, is completely unknown.

2022-04-01 | PXD015992 | Pride

Influenza virus infection leads to global cardiac proteome remodeling during convalescence

2022-04-04 | PXD016412 | Pride

Quantitative Proteomic and Phosphoproteomic Analyses of MLKL -/- mouse heart in response to influenza virus infection

2022-04-01 | PXD017936 | Pride

Transcriptomic Profiles of Multiple Organ Dysfunction Syndrome Phenotypes in Pediatric Critical Influenza

Project description:Influenza virus is responsible for a large global burden of disease, especially in children. Multiple Organ Dysfunction Syndrome (MODS) is a life-threatening and fatal complication of severe influenza infection. We measured RNA expression of 469 biologically plausible candidate genes in children admitted to North American pediatric intensive care units with severe influenza virus infection with and without MODS. Whole blood samples from 191 influenza-infected children (median age 6.4 years, IQR: 2.2, 11) were collected a median of 27 hours following admission; for 45 children a second blood sample was collected approximately seven days later. Extracted RNA was hybridized to NanoString mRNA probes, counts normalized, and analyzed using linear models controlling for age and bacterial co-infections (FDR q<0.05). Comparing pediatric samples collected near admission, children with Prolonged MODS for ≥7 days (n=38; 9 deaths) had significant upregulation of nine mRNA transcripts associated with neutrophil degranulation (RETN, TCN1, OLFM4, MMP8, LCN2, BPI, LTF, S100A12, GUSB) compared to those who recovered more rapidly from MODS (n=27). These neutrophil transcripts present in early samples predicted Prolonged MODS or death when compared to patients who recovered, however in paired longitudinal samples, they were not differentially expressed over time. Instead, five genes involved in protein metabolism and/or adaptive immunity signaling pathways (RPL3, MRPL3, HLA-DMB, EEF1G, CD8A) were associated with MODS recovery within a week. Thus, early increased expression of neutrophil degranulation genes indicated worse clinical outcomes in children with influenza infection, consistent with reports in adult cohorts with influenza, sepsis, and acute respiratory distress syndrome.

2023-07-07 | GSE236877 | GEO

Influenza virus infection leads to global proteome remodeling of Streptococcus pneumoniae

Project description:Our understanding of the synergism between S. pneumoniae and influenza virus remains incomplete. The classic dogma has been that influenza attenuates the host innate immunity and increase the susceptibility to subsequent bacterial infection. Therefore, the majority of current studies have been focusing on the interaction of S. pneumoniae and influenza in the context of host cells. By contrast, in this study, we set out to investigate the response of pneumococcus alone to virus infection. Our hypothesis was that prior to causing any damages to host cells, influenza may have induced (lethal) changes to pneumococcus cell itself. Indeed, a very recent evidence has shown that direct viral treatment to pneumococcus will increase its adhesion to macrophage cells. Here, using quantitative shotgun approach, we attempt to investigate the proteomic alterations of S. pneumoniae by influenza virus challenge, and provide a landscape of interactions between the IAV and pneumococcus.

2022-12-09 | PXD016122 | Pride

Phosphoproteomic characterization of Streptococcus pneumoniae and Influenza A virus synergism

Project description:Our understanding of the synergism between S. pneumoniae and influenza virus remains incomplete. The classic dogma has been that influenza attenuates the host innate immunity and increase the susceptibility to subsequent bacterial infection. Therefore, the majority of current studies have been focusing on the interaction of S. pneumoniae and influenza in the context of host cells. By contrast, in this study, we set out to investigate the response of pneumococcus alone to virus infection. Our hypothesis was that prior to causing any damages to host cells, influenza may have induced (lethal) changes to pneumococcus cell itself. Indeed, a very recent evidence has shown that direct viral treatment to pneumococcus will increase its adhesion to macrophage cells. Here, using quantitative phosphoproteomic approach, we attempt to investigate the global alterations of S. pneumoniae phosphorylation by influenza virus challenge, and provide a landscape of synergism between the IAV and pneumococcus.

2022-12-09 | PXD016214 | Pride

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

Elimination of fukutin reveals cellular and molecular pathomechanisms in muscular dystrophy-associated heart failure

Project description:Heart failure is the major cause of death for muscular dystrophy patients; however, the molecular pathomechanism remains unknown. Here, we show the detailed molecular pathogenesis of muscular dystrophy-associated cardiomyopathy in mice lacking the fukutin gene (Fktn), the causative gene for Fukuyama muscular dystrophy. Although cardiac Fktn elimination markedly reduced alpha-dystroglycan glycosylation and dystrophin-glycoprotein complex proteins in sarcolemma at all developmental stages, cardiac dysfunction was observed only in later adulthood, suggesting that membrane fragility is not the sole etiology of cardiac dysfunction. During young adulthood, Fktn-deficient mice were vulnerable to pathological hypertrophic stress with downregulation of Akt and the MEF2-histone deacetylase axis. Acute Fktn elimination caused severe cardiac dysfunction and accelerated mortality with myocyte contractile dysfunction and disordered Golgi-microtubule networks, which were ameliorated with colchicine treatment. These data reveal fukutin is crucial for maintaining myocyte physiology to prevent heart failure, and thus, the results may lead to strategies for therapeutic intervention.

2019-11-08 | GSE138280 | GEO

Discovery of drugs to treat cytokine storm-induced cardiac dysfunction

Project description:SARS-CoV2 infection leads to cardiac injury and dysfunction in 20-30% of hospitalized patients and higher rates of mortality in patients with pre-existing cardiovascular disease. Inflammatory factors released as part of the 'cytokine storm' are thought to play a critical role in cardiac dysfunction in severe COVID-19 patients. Here we use human cardiac organoid technology combined with high sensitivity phosphoproteomics and single nuclei RNA sequencing to identify inflammatory targets inducing cardiac dysfunction. This new pipeline allowed rapid progress and identification of putative therapeutics. We identify a novel interferon-gamma driven BRD4 (bromodomain protein 4)-fibrosis/iNOS axis as a key intracellular mediator of inflammation-induced cardiac dysfunction. This axis is therapeutically targetable using BRD4 inhibitors, which promoted full recovery of function in human cardiac organoids and prevented severe inflammation and death in a cytokine-storm mouse model. The BRD inhibitor INCB054329 was the most efficacious, and is a prime candidate for drug repurposing to attenuate cardiac dysfunction and improve COVID-19 mortality in humans.

2022-02-21 | PXD020994 | Pride

Transcriptomes of several organs of lean and obese mice infected with avian influenza

Project description:Influenza A virus (IAV) causes a wide range of extra-respiratory complications, ranging from central nervous system disease to cardiac disease. Obesity/overweight has previously been identified as a susceptibility factor for both severe influenza and cardiac disease. We therefore sought to investigate the systemic pathogenesis of influenza in an obese mouse model with a focus on cardiac complications of influenza.

2020-04-14 | GSE134685 | 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