Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Multi-organ profiles of respiratory syncytial virus (RSV)-infected BALB/c mice

ABSTRACT: Respiratory syncytial virus (RSV) a leading cause of pediatric and adult morbidity and mortality worldwide. It can cause complications in multiple organs, thus increasing hospital stays and costs. However, RSV-based studies have primarily focused on effects in the lungs and blood, thereby potentially neglecting critical genes and pathways. Hence, studying RSV infection via a novel multi-organ approach is important. In this study, lung, intestine, brain, and spleen tissues from six BALB/c mice (6–8 weeks old; three in control group and three in RSV-infected group) were subjected to RNA sequencing. Differentially expressed genes (DEGs) in each organ were obtained and functional enrichment analysis was performed. We first used CIBERSORT to evaluate the immune-infiltration landscape. Subsequently, common DEGs (co-DEGs) among the four organs were analyzed to identify key genes and pathways. After quantitative reverse transcription-polymerase chain reaction, western blotting, and external validation analysis of key hub genes, their correlation with immune cells and potential functions were explored. We found that the host response to RSV infection varied among the four organs regarding gene expression profiles and immune cell infiltration. Analysis of the 16 co-DEGs indicated enrichment in the platelet and neutrophil degranulation pathways. Importantly, the key gene hemopexin (Hpx) was strongly correlated with the immune cell fraction in the lungs and may participate in the regulation of platelet activation and immune response.

ORGANISM(S): Mus musculus

PROVIDER: GSE197868 | GEO | 2022/04/24

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Recombinant RSV G protein vaccine induces enhanced respiratory disease via IL-13 and mucin overproduction

Project description:The G protein expressed on the surface of respiratory syncytial virus (RSV) is important for adhesion to host cells and as a vaccine target antigen. The corresponding vaccines can effectively eliminate RSV, but exacerbate pulmonary immunopathology, such as eosinophil infiltration into the lungs, after the RSV challenge in animal models, raising concerns about enhanced respiratory disease (ERD), creating a need for approaches that mitigate these effects. Herein, we aimed to examine the mechanisms of G protein vaccine-induced ERD in mice, using recombinant G protein as a vaccine antigen. After the RSV challenge, G protein-vaccinated mice exhibited lung weight gain, lung tissue damage, and increased infiltration of eosinophils, neutrophils, and CD4+ T cells into the lungs. We set lung weight gain as the endpoint for ERD and examined the impact of each infiltrating cell on lung weight gain. We observed that CD4+ T cells, but not eosinophils or neutrophils, that infiltrate the lungs are responsible for lung weight gain. In addition, T helper 2 cell-mediated IL-13 induced mucin hypersecretion and lung weight gain. Mucin hypersecretion may contribute to weight gain in the lungs. In conclusion, our results indicate a novel mechanism of G protein vaccine-induced ERD via IL-13 and mucin hypersecretion, which could lead to the development of safe G protein vaccines and the elucidation of the causes of ERD associated with other vaccines.

2024-10-16 | GSE272499 | GEO

HuR coordinates systemic aging through platelet infiltration

Project description:Aging involves morphological and functional changes across different organs, but how these changes are linked among the different organs remains to be elucidated. Here, we uncover a central role of platelets in sys temic aging. In aged mice, the levels of platelet secreted pro inflammatory factors (PSPF) increased greatly in the serum and platelets, leading to a diffuse increase of platelet infiltration in brain, liver, lung, kidney, and aortic root. The RNA binding protein HuR/ELAVL1, a major regulator of R NA metabolism, promoted the production of PSPF in platelets. Platelet specific deletion of HuR reduced the expression of PSPF in platelets, alleviated platelet infiltration in brain, liver, lung, kidney, and aortic root, and delayed systemic aging. Our findings highlight a role of platelets in coordinating aging traits across organs.

2024-11-16 | GSE281572 | GEO

Gene expression in liver and lung of a high-fat diet fed, metastasizing mammary tumor-bearing and obesity-resistant mice

Project description:We explored early changes in gene expression in the livers and lungs of the HFD-fed, metastasizing mammary tumor-bearing and obesity-resistant mice mice. These alterations may have led to favorable conditions for both the formation of pro-inflammatory and pro-mitotic microenvironments in the target organs that promote immune cell infiltration and differentiation, as well as infiltration and proliferation of metastatic tumor cells. Total RNA was isolated from hepatic and pulmonary tissues of high fat diet fed-4T1 cell-injected mice or high fat diet fed-sham mice. Gene expressions were compared to control diet fed-same conditional mice.

2012-03-05 | E-GEOD-36211 | biostudies-arrayexpress

Gene expression in liver and lung of a high-fat diet fed, metastasizing mammary tumor-bearing and obesity-resistant mice

2012-03-05 | GSE36211 | GEO

Host Transcriptomic responses to pneumonic plague reveal that Yersinia pestis inhibits both the initial adaptive and innate immune responses in mice

Project description:Pneumonic plague is the most deadly form of infection caused by Yersinia pestis and can progress extremely fast. However, our understanding on the host transcriptomic response to pneumonic plague is insufficient. Here, we used RNA-sequencing technology to analyze transcriptomic responses in mice infected with fully virulent strain 201 or EV76, a live attenuated vaccine strain lacking the pigmentation locus. Approximately 600 differentially expressed genes (DEGs) were detected in lungs from both 201- and EV76-infected mice at 12 hours post-infection (hpi). DEGs in lungs of 201-infected mice exceeded 2,000 at 48 hpi, accompanied by sustained large numbers of DEGs in the liver and spleen; however, limited DEGs were detected in those organs of EV-infected mice. Remarkably, DEGs in lungs were significantly enriched in critical immune responses pathways in EV76-infected but not 201-infected mice, including antigen processing and presentation, T cell receptor signaling among others. Pathological and bacterial load analyses confirmed the rapid systemic dissemination of 201-infection and the confined EV76-infection in lungs. Our results demonstrate that fully virulent Y. pestis strongly inhibits both the innate and adaptive immune responses that are substantially stimulated in a self-limited infection, which update our holistic views on the transcriptomic response to pneumonic plague.

2017-07-13 | GSE84341 | GEO

Effect of 8-oxoguanine DNA glycosylase 1 (OGG1) inhibitor on pro-inflammatory gene expression.

Project description:Balbc J mouse received vehicle (solvent) or OGG1 inhibitor 1, 4, 8, 12, 24, 28 , 32, 36, 40 and 44h after RSV infection via intraperitoneal route. RSV (10^6 PFU) was installed into lungs via intranasal route in 60 microliters of solvent). One, 2, 3, 6, 12, 24, 48 and 72 hour after RSV challenge mice were sacrificed, lungs were removed and RNAs were isolated from individual lungs (n=6) After reverse transcription cDNAs were pooled and changes in gene expression was determined by using SABiosciences Mouse Inflammatory Cytokines & Receptors PCR Array (PAMM-011ZD)

2021-09-14 | GSE157630 | GEO

Transcription profiling of mouse lungs between vaccine-induced and natural immunity after Respiratory Syncytial Virus infection.

Project description:Transcriptional responses in lungs of mice infected with RSV upon primary, secondary, and vaccin-induced immunity

2010-10-20 | E-TABM-826 | biostudies-arrayexpress

Dexamethasone inhibits respiratory syncytial virus-driven mucus production while increasing viral replication without altering antiviral interferon signaling

Project description:Purpose: To understand how dexamethasone has beneficial effects on reducing mucus production but inhibits viral defense mechanisms Methods: RSV-infected mouse lungs and various cell lines, plus and minus dexamethason, were examined by RNAseq, and pathway analysis of differentially-expressed genes were compared Results: Using RNA-seq we identified a subset of cytokines that were induced by RSV and repressed by dexamethasone. Interestingly, while RSV induced interferons (IFNs) and IFN stimulated genes (ISGs), dexamethasone treatment did not affect the expression of these genes or antiviral IFN signaling pathways as has been observed with glucocorticoid treatment of other respiratory viruses [13]. Using an unbiased approach, we found that certain RSV-driven gene expression networks and genes were specifically modulated by dexamethasone treatment. Importantly, dexamethasone also reduced RSV clearance in vivo, which correlated with a reduction in specific immune response markers. Conclusion: Our results support the possibility that the beneficial anti-inflammatory effects of dexamethasone treatment are counterbalanced by the increased viral load in patients, accounting for the lack of clinical benefit derived from treatment during RSV infection.

2019-11-19 | GSE140226 | GEO

Transcription profiling of lung and bronchial lymph node from mice infected with Respiratory Syncytial Virus (RSV)

Project description:Transcriptional responses in lungs of mice infected with Respiratory Syncytial Virus (RSV) were compared to a control and mock infections

2007-04-17 | E-TABM-221 | biostudies-arrayexpress

NBEAL2 interactome: comparison between healthy donors and grey platelet syndrome (NBEAL2 deficient) patients activated T cells samples.

Project description:Loss of NBEAL2 function leads to grey platelet syndrome (GPS), a bleeding disorder characterized by macro-thrombocytopenia and α-granule-deficient platelets. A proportion of patients with GPS develop autoimmunity through an unknown mechanism, which might be related to the proteins NBEAL2 interacts with, specifically in immune cells. Here we show a comprehensive interactome of NBEAL2 in primary T cells, based on mass spectrometry identification of altogether 76 protein association partners. These include LRBA, a member of the same BEACH domain family as NBEAL2, recessive mutations of which cause autoimmunity and lymphocytic infiltration through defective CTLA-4 trafficking

2023-05-12 | PXD042180 | JPOST Repository

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