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RNAseq analysis of ileal transcriptomes to understand the effect of humoral immunodeficiency on small intestinal mucosal homeostasis

ABSTRACT: RNAseq analysis of ileal transcriptomes to understand the effect of humoral immunodeficiency on small intestinal mucosal homeostasis

PROVIDER: PRJNA773787 | ENA |

REPOSITORIES: ENA

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RNAseq analysis of ileal transcriptomes to understand the effect of humoral immunodeficiency on small intestinal mucosal homeostasis

Project description:Objective: The objective of this study was to more fully chracterize an inflammatory small intestinal enteropathy observed in CD19-/- mice (a model of humoral immunodeficiency). RNAseq was performed to characterize ileal transcriptomes pf WT and CD19-/- mice under steady-state conditions.

2021-12-16 | GSE186435 | GEO

RNAseq analysis of liver transcriptomes to understand the effect of humoral immunodeficiency on liver function

Project description:RNAseq analysis of liver transcriptomes to understand the effect of humoral immunodeficiency on liver function

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RNAseq analysis of liver transcriptomes to understand the effect of humoral immunodeficiency on liver function

Project description:Objective: The objective of this study was to understand how humoral immuno-deficiency influences molecular crosstalk between the ileum and liver, and liver bile acid metabolism. RNAseq was performed to characterize liver transcriptomes pf WT and CD19-/- mice under steady-state conditions.

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Rhesus macaque ileal loop study

Project description:Salmonella enterica serotype Typhimurium cause a localized enteric infection in immunocompetent patients while human immunodeficiency virus (HIV)-infected patients develop a life threatening bacteremia. We used a rhesus macaque ileal loop model to study how simian immunodeficiency virus (SIV) infection triggers defects in mucosal barrier function that enhance S. Typhimurium dissemination. SIV infection resulted in significant depletion of CD4+ T cells in the intestinal mucosa. Gene expression profiling revealed a defective TH17 response (with suppression of IL-17 and IL-22 expression) and impaired homeostasis of the intestinal epithelium in SIV-infected animals during NTS infection. These findings correlated with an impaired ability of lamina propria CD4+ T cells from SIV-infected macaques to produce IL-17 upon ex vivo stimulation, while production of IFNï§ was not affected. This cytokine imbalance in SIV-infected animals was associated with reduced expression of genes required for intestinal epithelial maintenance and repair, increased fluid secretion during NTS infection, epithelial damage and translocation of a non-invasive S. Typhimurium mutant. Although no defects in neutrophil recruitment were noted, the ileum of SIV-infected animals contained lower levels of the enzyme myeloperoxidase, which may indicate defects in neutrophil killing capacity. S. Typhimurium was recovered in markedly increased numbers from the mesenteric lymph nodes of SIV-infected macaques, illustrating the increased potential for systemic dissemination during co-infection. Our data suggest that SIV-infection causes a multi-factorial defect in mucosal barrier function that promotes bacterial dissemination. Keywords: Disease state analysis Comparison of ileal gene expression profiles in SIV infected rhesus macaques in response to Salmonella challange.

2010-05-26 | E-GEOD-10567 | biostudies-arrayexpress

A host-adapted auxotrophic gut symbiont induces mucosal immunodeficiency:EDITED

Project description:gut symbionts and mucosal immunodeficiency

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Relating the transcriptome and microbiome by paired terminal ileal Crohn's disease

Project description:Management of terminal ileal Crohn's disease (CD) is difficult due to fibrotic prognosis and failure to achieve mucosal healing. A limited number of synchronous analyses have been conducted on the transcriptome and microbiome in unpaired terminal ileum tissues. Therefore, our study focused on the transcriptome and mucosal microbiome in terminal ileal tissues of CD patients with the aim of determining the role of cross-talk between the microbiome and transcriptome in the pathogenesis of terminal ileal CD. Mucosa-attached microbial communities were significantly associated with segmental inflammation status. Interaction-related transcription factors (TFs) are the panel nodes for crosstalk between the gene patterns and microbiome for terminal ileal CD. The transcriptome and microbiome in terminal ileal CD can be different related to local inflammatory status, and specific differentially expressed genes (DEGs) may be targeted for mucosal healing. TFs connect gene patterns with the microbiome by reflecting environmental stimuli and signals from microbiota.

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A host-adapted auxotrophic gut symbiont induces mucosal immunodeficiency

Project description:A host-adapted auxotrophic gut symbiont induces mucosal immunodeficiency

| PRJEB68096 | ENA

A host-adapted auxotrophic gut symbiont induces mucosal immunodeficiency

Project description:A host-adapted auxotrophic gut symbiont induces mucosal immunodeficiency

| PRJEB68337 | ENA

A host-adapted auxotrophic gut symbiont induces mucosal immunodeficiency

Project description:A host-adapted auxotrophic gut symbiont induces mucosal immunodeficiency

| PRJEB67774 | ENA

Rhesus macaque ileal loop study

Project description:Salmonella enterica serotype Typhimurium cause a localized enteric infection in immunocompetent patients while human immunodeficiency virus (HIV)-infected patients develop a life threatening bacteremia. We used a rhesus macaque ileal loop model to study how simian immunodeficiency virus (SIV) infection triggers defects in mucosal barrier function that enhance S. Typhimurium dissemination. SIV infection resulted in significant depletion of CD4+ T cells in the intestinal mucosa. Gene expression profiling revealed a defective TH17 response (with suppression of IL-17 and IL-22 expression) and impaired homeostasis of the intestinal epithelium in SIV-infected animals during NTS infection. These findings correlated with an impaired ability of lamina propria CD4+ T cells from SIV-infected macaques to produce IL-17 upon ex vivo stimulation, while production of IFN-gamma was not affected. This cytokine imbalance in SIV-infected animals was associated with reduced expression of genes required for intestinal epithelial maintenance and repair, increased fluid secretion during NTS infection, epithelial damage and translocation of a non-invasive S. Typhimurium mutant. Although no defects in neutrophil recruitment were noted, the ileum of SIV-infected animals contained lower levels of the enzyme myeloperoxidase, which may indicate defects in neutrophil killing capacity. S. Typhimurium was recovered in markedly increased numbers from the mesenteric lymph nodes of SIV-infected macaques, illustrating the increased potential for systemic dissemination during co-infection. Our data suggest that SIV-infection causes a multi-factorial defect in mucosal barrier function that promotes bacterial dissemination. Keywords: Disease state analysis

2008-02-21 | GSE10567 | GEO

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