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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse IEC cell line gene expression

ABSTRACT: This SuperSeries is composed of the following subset Series:; GSE5112: Gene expression induced by flagellin stimulation in IECs; GSE5113: Gene expression induced by flagellin stimulation in CD11c+ LPCs Experiment Overall Design: Refer to individual Series

ORGANISM(S): Mus musculus

SUBMITTER: Satoshi Uematsu

PROVIDER: E-GEOD-5119 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Detection of pathogenic intestinal bacteria by Toll-like receptor 5 on intestinal CD11c+ lamina propria cells.

Uematsu Satoshi S Jang Myoung Ho MH Chevrier Nicolas N Guo Zijin Z Kumagai Yutaro Y Yamamoto Masahiro M Kato Hiroki H Sougawa Nagako N Matsui Hidenori H Kuwata Hirotaka H Hemmi Hiroaki H Coban Cevayir C Kawai Taro T Ishii Ken J KJ Takeuchi Osamu O Miyasaka Masayuki M Takeda Kiyoshi K Akira Shizuo S

Nature immunology 20060709 8

Toll-like receptors (TLRs) recognize distinct microbial components and induce innate immune responses. TLR5 is triggered by bacterial flagellin. Here we generated Tlr5-/- mice and assessed TLR5 function in vivo. Unlike other TLRs, TLR5 was not expressed on conventional dendritic cells or macrophages. In contrast, TLR5 was expressed mainly on intestinal CD11c+ lamina propria cells (LPCs). CD11c+ LPCs detected pathogenic bacteria and secreted proinflammatory cytokines in a TLR5-dependent way. Howe ...[more]

PMID: 16829963

Similar Datasets

Project description:Gene expression induced by flagellin stimulation in IECs and CD11c+ LPCs

| PRJNA96615 | ENA

Gene expression induced by flagellin stimulation in CD11c+ LPCs

Project description:Microarray analysis of IECs from Tlr5+/+ and Tlr5-/- mice stimulated with either medium alone or flagellin (1 µg/ml); to elucidate TLR5-mediated immune responses in CD11c+ LPCs Keywords: ordered

2006-08-01 | GSE5113 | GEO

Mus musculus

Project description:Gene expression induced by flagellin stimulation in CD11c+ LPCs

| PRJNA104513 | ENA

Transcription profiling of muse flagellin stimulated CD11c+ LPCs

Project description:Microarray analysis of IECs from Tlr5+/+ and Tlr5â/â mice stimulated with either medium alone or flagellin (1 Âµg/ml); to elucidate TLR5-mediated immune responses in CD11c+ LPCs Experiment Overall Design: CD11c+ LPCs from Tlr5+/+ and Tlr5â/â mice were treated with or without flagellin (1 ïg/ml) for 4 h. Total RNA was extracted with an RNeasy kit (Qiagen), and purified using an Oligotex mRNA Kit (Pharmacia). Fragmented and biotin-labeled cDNA was synthesized from 100 ng purified mRNA using the Ovation Biotin System (Nugen), according to the manufacturerâs protocol. cDNA was hybridized to Affymetrix Murine Genome 430 2.0 microarray chips (Affymetrix) according to the manufacturerâs instructions. Hybridized chips were stained, washed and scanned using a GeneArray Scanner (Affymetrix). Data analysis was performed with Microarray Suite software (Version 5.0, Affymetrix) and GeneSpring software (Silicon Genetics).

2008-06-13 | E-GEOD-5113 | biostudies-arrayexpress

Mus musculus

Project description:Gene expression induced by flagellin stimulation in IECs

| PRJNA104511 | ENA

Gene expression induced by flagellin stimulation in IECs

Project description:Microarray analysis of IECs from Tlr5+/+ and Tlr5–/– mice stimulated with either medium alone or flagellin (1 µg/ml); to elucidate TLR5-mediated immune responses in IECs. Keywords: ordered

2006-08-01 | GSE5112 | GEO

Transcription profiling of mouse IECS response to flagellin stimulation

Project description:Microarray analysis of IECs from Tlr5+/+ and Tlr5â/â mice stimulated with either medium alone or flagellin (1 Âµg/ml); to elucidate TLR5-mediated immune responses in IECs. Experiment Overall Design: IECs from Tlr5+/+ and Tlr5â/â mice were treated with or without flagellin (1 ïg/ml) for 4 h. Total RNA was extracted with an RNeasy kit (Qiagen), and purified using an Oligotex mRNA Kit (Pharmacia). Fragmented and biotin-labeled cDNA was synthesized from 100 ng purified mRNA using the Ovation Biotin System (Nugen), according to the manufacturerâs protocol. cDNA was hybridized to Affymetrix Murine Genome 430 2.0 microarray chips (Affymetrix) according to the manufacturerâs instructions. Hybridized chips were stained, washed and scanned using a GeneArray Scanner (Affymetrix). Data analysis was performed with Microarray Suite software (Version 5.0, Affymetrix) and GeneSpring software (Silicon Genetics).

2008-06-13 | E-GEOD-5112 | biostudies-arrayexpress

RNA-seq of GR WT and GR DIM ileum/IEC with DEX, Zn and untreated controls

Project description:The cytokine TNF drives inflammatory diseases, e.g. Crohn disease. In a mouse model of TNF-induced systemic inflammatory response syndrome (SIRS), severe impact on intestinal epithelial cells (IECs) is observed. Zinc confers complete protection in this model. We found that zinc no longer protects in animals which lack glucocorticoids (GCs), or express mutant versions of their receptor GR in IECs, nor in mice which lack gut microbiota. RNA-seq studies in IECs showed that zinc caused reduction of expression of constitutive (STAT1-induced) interferon-stimulated response (ISRE) genes and Interferon Regulatory Factor (IRF) genes. Since some of these genes are involved in TNF-induced cell death in intestinal crypt Paneth cells, and since zinc has direct effects on the composition of the gut microbiota (such as several Staphylococcus species) and on TNF-induced Paneth cell death, we postulate a new zinc-related anti-inflammatory mechanism. Zinc modulates the gut microbiota, causing less induction of ISRE/IRF genes in crypt cells, less TNF-induced necroptosis in Paneth cells and less fatal evasion of gut bacteria into the system.

2020-09-07 | GSE156242 | GEO

C. rodentium remodels metabolism in IEC

Project description:The mechanisms by which the mouse pathogen Citrobacter rodentium triggers effacement of the brush border microvilli, colitis, hyperplasia and dysbiosis remain poorly understood. We investigated the impact of C. rodentium infection on the proteomic and metabolic landscapes of intestinal epithelial cells (IECs) in vivo using isobaric labeling proteomics and targeted metabolomics. We found that infection depletes proteins involved in butyrate uptake, glycolysis, TCA cycle, lipid metabolism and oxidative phosphorylation with aparallel, increased production of creatine/phosphocreatine and cholesterol. The evolving ecological niche within the infected gut was concomitant with a reduction in butyrate-producing commensal bacteria and expansion of Proteobacteria that can metabolize cholesterol. These changes coincide with the modulation of IEC transcription factors by C. rodentium, specifically phosphorylation of Kdm5a, demethylation of histone H3 (Lys-4) and cleavage of Srebp2. Taken together our results show that whilst engaging with the host in a race to control innate immune responses, C. rodentium and the changing microbiota shape the metabolism flow in IECs.

2018-01-10 | PXD005004 | Pride

IEC intrinsic IL-1R signaling holds dual roles in regulating intestinal homeostasis and inflammation

Project description:Introduction: Intestinal epithelial cells (IECs) constitute a critical first line of defense against microbes by providing a physical barrier capable of producing antimicrobial peptides (AMPs) and cytokines. While IECs are known to respond to various microbial signals, the precise upstream cues regulating diverse IEC responses are not clear. Method: Mouse intestinal crypts were isolated from colon tissue. Crypts were differentiated into 3D spheroids in matrigel by stimulating with LWRN media and growth factors. After differentiation colonoids were stimulated with IL-1b, IL-22, or IL-1b and IL-22 for 12 hours then RNA was isolated for RNA sequencing. Conclusion: Transcriptional profiling of mColonoids reveals IL-1b synergizes with IL-22 to induced a unique gene profile

2023-03-22 | GSE193267 | GEO

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