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Omics score: 0

E-GEOD-48125

ABSTRACT: Neonatal antibotic prophylaxis modulates intestinal immunity and prevents necrotizing enterocolitis in preterm neonates

OTHER RELATED OMICS DATASETS IN: PRJNA208962

TISSUE(S): Duodenum, Ileum

PROVIDER: E-GEOD-48125 | ExpressionAtlas | 2015-07-15

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-GEOD-48125-analysis-methods.tsv	Tabular
	E-GEOD-48125-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-48125-configuration.xml	Xml
	E-GEOD-48125-percentile-ranks.tsv	Tabular
	E-GEOD-48125.condensed-sdrf.tsv	Tabular

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Project description:Neonatal antibotic prophylaxis modulates intestinal immunity and prevents necrotizing enterocolitis in preterm neonates

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Dual RNA Seq of Salmonella-positive and Salmonella-negative small intestinal epithelial cells using the neonatal infection model

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IL-22 promotes postnatal formation of MUC17 glycocalyx barrier that protects host enterocytes

Project description:The apical aspects of absorptive epithelial cells form a highly organized brush border membrane (BBM), shaped by densely packed microvilli that are coated with a glycocalyx. Here, we present evidence showing that the glycocalyx forms an epithelial barrier that prevents exogenous molecules from gaining access to the BBM. We used a multiomics approach to investigate function and regulation of membrane mucins exposed on the enterocytic BBM during postnatal development of the small intestine. Muc17 was identified as a major membrane mucinin the glycocalyx that was specifically upregulated by IL-22 as part of an epithelial defense repertoire during suckling-weaning transition. High levels of IL-22 at the time of weaning primed progenitor enterocyte to express Muc17 as they migrate out of intestinal crypts to replace neonatal enterocytes. Our findings propose a role for membrane mucin Muc17 in epithelial barrier function in the small intestine.

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Project description:QRXZF modulates gut microbiota and prevents DKD.

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Transcription profiling of mouse virulence models to investigate urine host cell response to Aeromonas infection

Project description:Aims: To assess the virulence of multiple Aeromonas spp. using two models, a neonatal mouse assay and a mouse intestinal cell culture. Methods and Results: Transcriptional responses to both infection models were evaluated using microarrays. After artificial infection with a variety of Aeromonas spp., mRNA extracts from the two models were processed and hydridized to murine microarrays to determine host gene response. Definition of virulence was determined based on host mRNA production in murine neonatal intestinal tissue and mortality of infected animals. Infections of mouse intestinal cell cultures were then performed to determine whether this simpler model system's mRNA responses correlated to neonatal results and therefore be predictive of virulence of Aeromonas spp. Virulent aeromonads up-regulated transcripts in both models including multiple host defense gene products (chemokines, regulation of transcription and apoptosis, cell signaling). Avirulent species exhibited little or no host response in neonates. Mortality results correlated well with both bacterial dose and average fold change of up-regulated transcripts in the neonatal mice. Conclusions: Cell culture results were less discriminating but showed promise as potentially being able to be predictive of virulence. Jun oncogene up-regulation in murine cell culture is potentially predictive of Aeromonas virulence. Significance and Impact of the Study: Having the ability to determine virulence of waterborne pathogens quickly would potentially assist public health officials to rapidly assess exposure risks. Experiment Overall Design: Two infection models were assessed, live, whole animals (neonatal Swiss Webster mice) and a murine small intestinal cell culture. Biological replicates (n=5) were infected with different Aeromonas species/strains and compared to uninfected controls.

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Induced Endothelial Cell Cycle Arrest Prevents Arterio-venous Malformations in Hereditary Hemorrhagic Telangiectasia

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Microarray comparing gene expression changes between control, normoglycaemic mice, and mice expressing the human neonatal diabetes mutation Kir6.2-V59M in pancreatic beta-cells left diabetic for 2 weeks

Project description:Activating mutations in the KATP channel cause a rare genetic form of diabetes called neonatal diabetes. These mutations render the channel permanently open results in membrane hyperpolarisation of the pancreatic beta-cell. This prevents calcium influx and impairs insulin secretion. Mice expressing the human neonatal diabetes mutation Kir6.2-V59M specifically in pancreatic beta-cells are diabetic but do not display dyslipidaemia or insulin resistance. In this experiment, gene expression changes were analysed to explore the effect of high blood glucose per se on isolated pancreatic islets

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