Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Rotavirus susceptibility of antibiotic-treated mice ascribed to diminished expression of IL-22

ABSTRACT: We wanted to identify effector molecules which confer rotavirus resistance in microbiota-depleted mice We used microarrays to analyze the global programme of gene expression in response to IL22 treatment in the ileum of antibiotic-treated Ifnlr1-/- mice

ORGANISM(S): Mus musculus

PROVIDER: GSE166400 | GEO | 2021/08/03

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Rotavirus susceptibility of antibiotic-treated mice ascribed to diminished expression of interleukin-22.

Project description:The commensal microbiota regulates susceptibility to enteric pathogens by fine-tuning mucosal innate immune responses, but how susceptibility to enteric viruses is shaped by the microbiota remains incompletely understood. Past reports have indicated that commensal bacteria may either promote or repress rotavirus replication in the small intestine of mice. We now report that rotavirus replicated more efficiently in the intestines of germ-free and antibiotic-treated mice compared to animals with an unmodified microbiota. Antibiotic treatment also facilitated rotavirus replication in type I and type III interferon (IFN) receptor-deficient mice, revealing IFN-independent proviral effects. Expression of interleukin-22 (IL-22) was strongly diminished in the intestine of antibiotic-treated mice. Treatment with exogenous IL-22 blocked rotavirus replication in microbiota-depleted wild-type and Stat1-/- mice, demonstrating that the antiviral effect of IL-22 in animals with altered microbiome is not dependent on IFN signaling. In antibiotic-treated animals, IL-22-induced a specific set of genes including Fut2, encoding fucosyl-transferase 2 that participates in the biosynthesis of fucosylated glycans which can mediate rotavirus binding. Interestingly, IL-22 also blocked rotavirus replication in antibiotic-treated Fut2-/- mice. Furthermore, IL-22 inhibited rotavirus replication in antibiotic-treated mice lacking key molecules of the necroptosis or pyroptosis pathways of programmed cell death. Taken together, our results demonstrate that IL-22 determines rotavirus susceptibility of antibiotic-treated mice, yet the IL-22-induced effector molecules conferring rotavirus resistance remain elusive.

| S-EPMC8360596 | biostudies-literature

Rotavirus susceptibility of antibiotic-treated mice ascribed to diminished expression of IL-22

Project description:Rotavirus susceptibility of antibiotic-treated mice ascribed to diminished expression of IL-22

| PRJNA700697 | ENA

Rotavirus A

Project description:Rotavirus A Sequencing

| PRJNA221644 | ENA

Rotavirus

Project description:Rotavirus Genomics of African Stool Samples

| PRJNA201332 | ENA

Rotavirus A

Project description:Rotavirus A Genome sequencing

| PRJNA1114740 | ENA

Rotavirus A

Project description:Rotavirus in municipal wastewater

| PRJDB4513 | ENA

Rotavirus A

Project description:Rotavirus A Genome sequencing

| PRJNA539952 | ENA

Rotavirus

Project description:Enteric virome in rotavirus vaccine-derived cases

| PRJNA765185 | ENA

Rotavirus activates B but impairs T lymphocytes

Project description:Rotavirus infection is the single most important cause of severe diarrhea in young children worldwide. We used Affymetrix Human U95Av2 high density oligonucleotide arrays to compare gene expression profiles in peripheral blood mononuclear cells (PBMC) of 10 children with acute rotavirus diarrhea and 8 age-matched healthy children. We also examined patterns of gene expression in 5 convalescent-phase PBMC samples from rotavirus patients. For data analysis, we imported .cel files generated by Affymetrix MAS5.0 into Genetraffic 3.1 software (Iobion) and performed robust multi-chip analysis. We considered a gene in patients differentially expressed if its level of expression was at least 1.5-fold higher or lower than the baseline (arithmetic mean) of the corresponding gene in 8 controls and if its pattern of elevated or repressed expression was observed in at least 7 of the 10 patients. Using these criteria, we identified ~1% up- and ~2% down-regulated genes in acute-phase PBMC of patients. Up-regulated genes included those involved in the differentiation, maturation, activation, and survival of B cells, as well as an array of genes with function in inflammatory and antiviral activities. We observed a pattern of repressed expression of a number of genes involved in the various stages of T-cell development and activation. On the basis of these results, we conclude that rotavirus infection induces robust inflammatory response and B-cell activation but represses T-cell response. Keywords: other

2006-06-01 | GSE2729 | GEO

Murine rotavirus infects and replicates in intestinal tuft cells

Project description:RNAseq of coding and noncoding RNA isolated from intestinal tuft cells reveals murine rotavirus replication in intestinal tuft cells.

2021-10-04 | GSE168773 | 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