Gut microbiota and rotavirus
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ABSTRACT:
PROVIDER: PRJEB41221 | ENA |
REPOSITORIES: ENA
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Project description:Rotaviruses are recognized as the leading cause of severe dehydrating diarrhea in infants and young children worldwide. Preventive and therapeutic strategies are urgently needed to fight this pathogen. In tissue culture and in vivo, rotavirus induces structural and functional alterations in the host cell. In order to better understand the molecular mechanisms involved in the events after rotavirus infection, we identified host cellular genes whose mRNA levels changed after infection. For this analysis, we used microarrays containing more than 38,000 human cDNAs to study the transcriptional response of the human intestinal cell line Caco-2 to rotavirus infection. We found that 508 genes were differentially regulated >2-fold at 16 h after rotavirus infection, and only one gene was similarly regulated at 1 h postinfection. Of these transcriptional changes, 73% corresponded to the upregulation of genes, with the majority of them occurring late, at 12 or more hours postinfection. Some of the regulated genes were classified according to known biological function and included genes encoding integral membrane proteins, interferon-regulated genes, transcriptional and translational regulators, and calcium metabolism-related genes. A new picture of global transcriptional regulation in the infected cell is presented and families of genes which may be involved in viral pathogenesis are discussed. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Computed
2005-10-13 | E-GEOD-3442 | biostudies-arrayexpress
Project description:Rotaviruses are recognized as the leading cause of severe dehydrating diarrhea in infants and young children worldwide. Preventive and therapeutic strategies are urgently needed to fight this pathogen. In tissue culture and in vivo, rotavirus induces structural and functional alterations in the host cell. In order to better understand the molecular mechanisms involved in the events after rotavirus infection, we identified host cellular genes whose mRNA levels changed after infection. For this analysis, we used microarrays containing more than 38,000 human cDNAs to study the transcriptional response of the human intestinal cell line Caco-2 to rotavirus infection. We found that 508 genes were differentially regulated >2-fold at 16 h after rotavirus infection, and only one gene was similarly regulated at 1 h postinfection. Of these transcriptional changes, 73% corresponded to the upregulation of genes, with the majority of them occurring late, at 12 or more hours postinfection. Some of the regulated genes were classified according to known biological function and included genes encoding integral membrane proteins, interferon-regulated genes, transcriptional and translational regulators, and calcium metabolism-related genes. A new picture of global transcriptional regulation in the infected cell is presented and families of genes which may be involved in viral pathogenesis are discussed. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set
2005-10-13 | GSE3442 | GEO
Project description:To understand the impact of murine rotavirus infection on mouse intestinal epithelial tissue, we isolated total intestinal epithelium from uninfected and infected C57Bl6J mice and performed single-cell RNAseq.
2021-10-04 | GSE169197 | GEO
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
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.
2007-11-01 | E-GEOD-2729 | biostudies-arrayexpress
Project description:In a single-cell RNA sequencing experiment, we defined subsets of intestinal epithelial cells in 5-day-old mice and observed decreased transcript levels of sodium-hydrogen exchanger 3 (Nhe3) and Dra in several epithelial cell groups following rotavirus infection. In contrast, transcript levels of sodium-glucose cotransporter 1 (Sglt1), electrogenic sodium bicarbonate cotransporter (Nbce1), solute carrier family 12 member 2 (Nkcc1), and Cftr were unaffected. Furthermore, expression of Nhe3 and Dra was down-regulated in both rotavirus infected intestinal epithelial cells that contained rotavirus transcripts and uninfected bystander cells, suggesting induction of paracrine signaling.
2025-02-28 | GSE288639 | GEO
Project description:Intestinal epithelial cells (IECs) serve as both a physical barrier and a source of robust antiviral interferon (IFN) response. As such, they constitute the primary barrier that enteric viruses, such as rotavirus, need to overcome to initiate infection. The gut is characterized by very low oxygen levels (hypoxia) within the lumen, resulting in a unique hypoxic physiological environment in which rotavirus infection occurs. Depending on the tissues or viruses, conflicting results have been described for the role of hypoxia in regulating viral infections, where hypoxia could have either a proviral or antiviral function. Since intestinal epithelial cells naturally exist in a hypoxic environment, it is essential to investigate how these conditions affect rotavirus infection. We found that hypoxia promotes rotavirus infection, resulting in increased virus replication and production of infectious virus particles. We showed that this increased production of rotavirus particles under hypoxia is due to a decreased induction of both type I and III IFNs leading to a decreased expression of IFN stimulated genes (ISGs) and antiviral protection. RNA sequencing showed a robust decrease in ISG production in hypoxia for both rotavirus infection and poly I:C transfection, suggesting a conserved inhibition of IFN responses in hypoxia for IECs. Functional analyses revealed that hypoxia impairs signal transduction leading to IFN expression by negatively regulating the activation of the master signaling molecule TBK1. Mechanistically, we determined that hypoxia induces the expression of the protein phosphatase PP2A which is responsible for the hypoxia-induced impairment of TBK1 activation. Importantly, we observed that this hypoxia-mediated dampening of immune response was not restricted to rotavirus infection but dampened the IFN induction of a broad range of viruses and immune stimuli. Together, we propose that hypoxia creates an immune-suppressive environment through downregulation of IFN, representing a novel proviral mechanism for hypoxia in the human gastro-intestinal tract.
2025-11-13 | GSE300313 | GEO
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
Project description:Germ-free (GF) mice can be used as a powerful tool to investigate the role of the intestinal commensal flora in metabolism and immune tolerance. In this study we have used whole genome transcriptome analyses to compare expression levels systemically in liver of germ-free mice and specific pathogen free (SPF) mice. Keywords: Mouse liver tissue germ-free or specific pathogen free vs universal mouse reference Specific Pathogens Excluded from the SPF mice: Virus 1. Mouse Hepatitis Virus (MHV) 2. Mouse Rotavirus (EDIM) 3. Parvoviruses Minute virus of mice (MVM) Mouse parvo virus (MPV) 4. Pneumonia virus of mice (PVM) 5. Sendai virus 6. Theiler's encephalomyelitis virus 7. Ectromelia virus 8. Lymphocytic choriomeningitis virus (LCMV) 9. Mouse adenovirus 10. Mouse cytomegalovirus 11. Reovirus type 3 Bacteria 1. Citrobacter rodentium 2. Clostridium piliforme (Tyzzer’s disease) 3. Corynebacterium kutscheri 4. Mycoplasma pulmonis 5. Pasteurellaceae 6. Salmonella spp. 7. Streptococci-β-haemolytic 8. Streptococcus pneumoniae 9. Helicobacter spp. 10. Streptobacillus moniliformis Parasite 1. Ectoparasites 2. Endoparasites
2009-09-22 | GSE14689 | GEO