Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Molecular landscape of respiratory infection: A large-scale, multi-centre blood transcriptome dataset

ABSTRACT: Respiratory infections pose significant challenges to global health, impacting millions of individuals annually. Understanding the molecular mechanisms underlying the pathogenicity of these infections is crucial for developing effective interventions. RNA sequencing provides insights into a patient’s global transcriptome changes, facilitating the identification of host gene signatures in response to infection and potential therapeutic targets. Here we present an extensive whole blood transcriptome dataset from a demographically diverse cohort of 502 patients with infections including COVID-19, seasonal coronavirus, influenza A or influenza B, sepsis, septic shock, and co-infections (Viral/Viral, Bacterial/Viral, Bacterial/Viral/Fungal, Viral/Fungal, Viral/ Viral/Fungal).

ORGANISM(S): Homo sapiens

PROVIDER: GSE282464 | GEO | 2025/03/26

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

STAT2 Signaling Regulates Macrophage Phenotype during Influenza and Bacterial Super-infection

Project description:Influenza is the common respiratory problem that infects between 5-20% of the US population and results in 30,000 deaths annually. A primary cause of the influenza-associated death is due to secondary bacterial pneumonia. In this study, we investigated the role of STAT2 signaling during influenza and influenza-bacterial super-infection in mice. Herein, we demonstrate that STAT2 signaling is required for viral control, regulation of inflammation, and limiting mortality during influenza single infection. Surprisingly, despite this deficiency in anti-viral immunity, we found increased bacterial control and survival in STAT2 deficient mice during influenza-MRSA super-infection compared to controls. This protection in the absence of STAT2 was associated with accumulation of dual phenotype M1/M2 macrophages, which were required for control of bacterial infection. Together, these results suggest that the STAT2 signaling is involved in suppressing macrophage activation and bacterial control during influenza-bacterial super-infection.

2018-12-26 | GSE119029 | GEO

Antibiotic use during influenza infection augments lung eosinophils that impair lung immunity against secondary bacterial pneumonia

Project description:A leading cause of morbidity and mortality during influenza infection is the development of a secondary bacterial pneumonia, which is appropriately treated with antibiotics. In the absence of a bacterial superinfection, prescribing antibiotics is not indicated but has nevertheless become a common clinical practice for those presenting with a respiratory viral illness. We found that antibiotic use during an antecedent influenza infection impaired the lung innate immunologic defenses toward a secondary challenge with methicillin-resistantStaphylococcus aureus(MRSA). The antibiotics perturbed the gut microbiome causing a fungal dysbiosis that drives an increase in lung eosinophils. We also demonstrate eosinophils, through the release of major basic protein, impair macrophage ability to clear MRSA. Moreover, we provide clinical evidence that eosinophils positively correlate with antibiotic use and worsened outcomes in patients hospitalized for viral infections. Altogether, our work establishes a counterproductive effect of antibiotic treatment during influenza infection that have negative immunologic consequences in the lungs thereby increasing the risk of developing a secondary bacterial infection.

2024-08-21 | GSE259429 | GEO

Fungal Dysbiosis in Post-Influenza MRSA Infection

2024-08-21 | GSE243542 | GEO

Pathogen Class-specific Transcriptional Responses Derived from PBMCs Accurately Discriminate Between Fungal, Bacterial, and Viral Infections [ValidationCohort]

Project description:Host gene expression responses can be used to determine the etiology of acute infection. PBMCs were stimulated with bacterial, viral, and fungal stimuli and then analyzed for differential gene expression utilizing microarrays to derive pathogen class-specific gene expression classifiers of infection. Validation Cohort: peripheral blood samples of human patients with acute viral, bacterial, or fungal infections

2024-09-28 | GSE277849 | GEO

Cell-intrinsic regulation of phagocyte function by interferon lambda during pulmonary viral, bacterial super-infection

Project description:Influenza infections result in a significant number of severe illnesses annually, many of which are complicated by secondary bacterial super-infection. Primary influenza infection has been shown to increase susceptibility to secondary methicillin-resistant Staphylococcus aureus (MRSA) infection by altering the host immune response, leading to significant immunopathology. Type III interferons (IFNs), or IFNλs, have gained traction as potential antiviral therapeutics due to their restriction of viral replication without damaging inflammation. The role of IFNλ in regulating epithelial biology in super-infection has recently been established; however, the impact of IFNλ on immune cells is less defined. In this study, we infected wild-type and IFNLR1-/- mice with influenza A/PR/8/34 followed by S. aureus USA300. We demonstrated that global IFNLR1-/- mice have enhanced bacterial clearance through increased uptake by phagocytes, which was shown to be cell-intrinsic specifically in myeloid cells in mixed bone marrow chimeras. We also showed that depletion of IFNLR1 on CX3CR1 expressing myeloid immune cells, but not neutrophils, was sufficient to significantly reduce bacterial burden compared to mice with intact IFNLR1. These findings provide insight into how IFNλ in an influenza-infected lung impedes bacterial clearance during super-infection and show a direct cell intrinsic role for IFNλ signaling on myeloid cells.

2024-08-15 | GSE268994 | GEO

The global Proteome and Ubiquitinome of bacterial and viral co-infected Bronchial Epithelial Cells

Project description:Viral infections facilitate bacterial trafficking to the lower respiratory tract resulting in bacterial viral co infections. Bacterial dissemination to the lower respiratory tract is enhanced by influenza A virus induced epithelial cell damage and dysregulation of immune responses. Epithelial cells act as the first line of defense and detect pathogens by a high variety of pattern recognition receptors. The post translational modification ubiquitin is involved in almost every cellular process. Moreover, ubiquitination contributes to the regulation of host immune responses, influenza A virus uncoating and transport within host cells. We applied proteomics with a special focus on ubiquitination to assess the impact of single bacterial and viral as well as bacterial viral co-infections on bronchial epithelial cells. We used Tandem Ubiquitin Binding Entities to enrich polyubiquitinated proteins and assess changes in the ubiquitinome. Infecting 16HBE cells with Streptococcus pyogenes led to an increased abundance of proteins related to mitochondrial translation and energy metabolism in proteome and ubiquitinome. In contrast, influenza A virus infection mainly altered the ubiquitinome. Co-infections had no additional impact on protein abundances or affected pathways. Changes in protein abundance and enriched pathways were assigned to imprints of both infecting pathogens.

2022-02-24 | PXD025146 | Pride

Differential ability of pandemic and seasonal H1N1 influenza 1 A virus to alter function of human neutrophils

Project description:Neutrophils are essential cells of host innate immunity. Although the role of neutrophils in defense against bacterial and fungal infections is well characterized, there is relative paucity of information about their role against viral infections. Influenza A virus (IAV) infection can be associated with secondary bacterial co-infection, and it has long been posited that the ability of IAV to alter normal neutrophil function predisposes individuals to secondary bacterial infections. To better understand this phenomenon, we evaluated the interaction of pandemic or seasonal H1N1 IAV with human neutrophils isolated from healthy subjects. These viruses were ingested by human neutrophils and elicited changes in neutrophil gene expression that are consistent with an interferon-mediated immune response. Viability of neutrophils following co-culture with either pandemic and seasonal H1N1 IAV was similar for up to 18 h of culture. Notably, neutrophil exposure to seasonal IAV (but not pandemic IAV) primed these leukocytes for enhanced functions, including production of reactive oxygen species and bactericidal activity. Taken together, our results are at variance with the universal idea that IAV impairs neutrophil function directly to predispose individuals to secondary bacterial infections. Rather, we suggest some strains of IAV prime neutrophils for enhanced bacterial clearance.

2017-12-05 | GSE100865 | GEO

FLUNEXT transcriptome analysis

Project description:Influenza virus infections remain a major public health burden. The intrinsic ever-evolving nature of this virus, the suboptimal efficacy of recent influenza inactivated vaccines, as well as the emergence of resistance against a limited antiviral arsenal, highlight the urgent need for novel therapeutic approaches to treat influenza infections. Here, we exploited in vivo transcriptomic signatures of infection, directly obtained from a patient’s cohort to identify in silico a list of marketed drugs with signatures that counteracted that of the infection state.

2019-02-13 | GSE93731 | GEO

The global Proteome and Ubiquitinome of bacterial and viral co-infected Bronchial Epithelial Cells

2022-06-13 | PXD026625 | panorama

Pathogen Class-specific Transcriptional Responses Derived from PBMCs Accurately Discriminate Between Fungal, Bacterial, and Viral Infections [DiscoveryCohort]

Project description:Host gene expression responses can be used to determine the etiology of acute infection. PBMCs were stimulated with bacterial, viral, and fungal stimuli and then analyzed for differential gene expression utilizing microarrays to derive pathogen class-specific gene expression classifiers of infection. Discovery Cohort: In vitro human PBMC challenges were performed with bacteria (gram postive and gram negative), viruses (4 strains of influenza), and fungi (Cryptococcus and Candida)

2024-09-28 | GSE277848 | 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