Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Transcription profiling of mouse (SCID) after intestinal xenotransplants infected with Shigella

ABSTRACT: to analyse the transcriptomic response of human intestinal tissue engrafted in SCID mice to Shigella infection Experiment Overall Design: Four experimental conditions with two biological replicates. Experiment Overall Design: After 2 hours infection, tissues were removed and ARN were extracted before labeling and hybridizations on U-133A genechip.

ORGANISM(S): Homo sapiens

SUBMITTER: Thierry Pedron

PROVIDER: E-GEOD-8636 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Virulent Shigella flexneri subverts the host innate immune response through manipulation of antimicrobial peptide gene expression.

Sperandio Brice B Regnault Béatrice B Guo Jianhua J Zhang Zhi Z Stanley Samuel L SL Sansonetti Philippe J PJ Pédron Thierry T

The Journal of experimental medicine 20080421 5

Antimicrobial factors are efficient defense components of the innate immunity, playing a crucial role in the intestinal homeostasis and protection against pathogens. In this study, we report that upon infection of polarized human intestinal cells in vitro, virulent Shigella flexneri suppress transcription of several genes encoding antimicrobial cationic peptides, particularly the human beta-defensin hBD-3, which we show to be especially active against S. flexneri. This is an example of targeted ...[more]

PMID: 18426984

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Project description:Phosphorylation of histone H3 at Serine 10 emerges as a mechanism increasing chromatin accessibility of the transcription factor NF-kB for a particular set of immune genes. Here we report that a bacterial pathogen uses this strategy to shape the transcriptional response of infected host cells. We identify the Shigella flexneri type III protein effector OspF as a Dual Specific Phosphatase. OspF dephosphorylates MAP kinases within the nucleus impairing histone H3 phosphorylation at Serine 10 in a gene-specific manner. Therefore, OspF reprograms the transcriptional response for inactivation of a subset of NF-kB responsive genes. This regulation leads to repression of polymorphonuclear leukocytes recruitment in infected tissues. Thus, pathogens have evolved the ability to precisely modulate host cell epigenetic information as a strategy to repress innate immunity. Experiment Overall Design: The wild-type (WT) invasive strain of S. flexneri serotype 5a. To construct the ospF mutant, a PCR amplified DNA fragment encompassing nucleotides 61 to 420 of ospF was cloned between the XbaI and EcoRI sites of the suicide plasmid pSW23T, giving raise to pSWOspFTr. This plasmid was transferred by conjugation to the WT strain WT-Sm. To complement the ospF mutant, we constructed pUC18-OspF containing a PCR fragment encompassing the ospF gene inserted between the EcoRI and HindIII sites of pUC18. Experiment Overall Design: Cells were infected 2 hours with the differents strains. 2 biological replicates were done for each experimental conditions. After infection, cells were washed and total RNA was extracted using Rneasy mini kit from Qiagen. After cRNA synthesis and labeling with biotin, hybridizations were performed following Affymetrix procedures. After scanning, data were normalized with RMA (Quantile normalization). Experiment Overall Design: Comparative analyses with dChip software between baseline (wild-type-infected cells) and experiment (mutant- or transcomplemented strain-infected cells) were done using an unpaired Welch t-test with a p-value threshold of 0.05 and a Signal Log Ratio (SLR) threshold of 0.6. This SLR threshold corresponds to a Fold Change of 1.5

Dataset Information

Transcription profiling of mouse (SCID) after intestinal xenotransplants infected with Shigella

Publications

Virulent Shigella flexneri subverts the host innate immune response through manipulation of antimicrobial peptide gene expression.

Similar Datasets

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