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Expression data from CD4+ T cells of germ free mice, SPF IQI mice and SPF C57BL/6 mice depletd with Uhrf1 (by Cd4Cre-Uhrf1flox/flox)

ABSTRACT: Commensal bacteria shapes gut immune system. Colonization bacteria increase the frequency of regulatory T cells, however, the molecular mechanisms has not yet been unknown. To reveal the mechanism, we isolated Treg cells and Non-Treg cells and performed the global expression analysis.

ORGANISM(S): Mus musculus

PROVIDER: GSE56542 | GEO | 2014/04/07

SECONDARY ACCESSION(S): PRJNA243859

REPOSITORIES: GEO

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Expression data from CD4+ T cells of germ free mice, SPF IQI mice and SPF C57BL/6 mice depletd with Uhrf1 (by Cd4Cre-Uhrf1flox/flox)

Project description:Commensal bacteria shapes gut immune system. Colonization bacteria increase the frequency of regulatory T cells, however, the molecular mechanisms has not yet been unknown. To reveal the mechanism, we isolated Treg cells and Non-Treg cells and performed the global expression analysis. Colonic lamina propria cells were isolated from mice described above. Treg cells and Non-Treg cells (also called as Tconv cells) were sorted by FACS AriaIII

2014-04-07 | E-GEOD-56542 | biostudies-arrayexpress

Expression data from CD4+ T cells of germ free mice, SPF IQI mice and SPF C57BL/6 mice depletd with Uhrf1

Project description:Commensal bacteria shapes gut immune system. Colonization bacteria increase the frequency of regulatory T cells, however, the molecular mechanisms has not yet been unknown. To reveal the mechanism, we isolated Treg cells and Non-Treg cells and performed the global expression analysis. Colonic lamina propria cells were isolated from mice described above. Cells were divided into Treg or Non-Treg cells by FACS AriaIII

2015-06-10 | E-GEOD-47818 | biostudies-arrayexpress

Expression data from CD4+ T cells of germ free mice, SPF IQI mice and SPF C57BL/6 mice depletd with Uhrf1

2015-06-10 | GSE47818 | GEO

RNA-seq mouse intestines from PN, Germ-free, SPF and Antibiotics-treated mice

Project description:We hypothesized that there were genes involved in the maintenance of intestinal tolerance to commensal bacteria. These genes should meet the following criteria: expressed in intestines, upregulated in the presence of commensal bacteria and downregulated in absence of microbes. To find these genes, we collected small intestines from postnatal mice that neither affected by the bacteria nor by the food, adult mice bred in germ-free or specific pathogen-free conditions, and adult SPF mice treated with antibiotics. We therefore performed bulk RNA sequencing using these cells.

2023-01-01 | E-MTAB-12215 | biostudies-arrayexpress

Expression data from CD4+ Naïve T cells under Treg-inducing condition in the presence or absence of butyrate

Project description:Commensal bacteria shapes gut immune system. Colonization bacteria increase the frequency of regulatory T cells, however, the molecular mechanisms has not yet been unknown. To reveal the mechanism, we isolated Naïve CD4+ T cells from spleen of C57BL/6 mice and cultured the cells under Treg-inducing condition culture in the presence or absence of butyrate, a metabolite produced by commensal bacteria.

2013-11-20 | GSE49619 | GEO

Expression data from CD4+ NaM-CM-/ve T cells under Treg-inducing condition in the presence or absence of butyrate

Project description:Commensal bacteria shapes gut immune system. Colonization bacteria increase the frequency of regulatory T cells, however, the molecular mechanisms has not yet been unknown. To reveal the mechanism, we isolated NaM-CM-/ve CD4+ T cells from spleen of C57BL/6 mice and cultured the cells under Treg-inducing condition culture in the presence or absence of butyrate, a metabolite produced by commensal bacteria. NaM-CM-/ve T cells were isolated from spleen and were cultured in the presence of IL-2, TGF-beta and in the presence or absene of Butyrate. RNA was extracted at Day 2

2013-11-20 | E-GEOD-49619 | biostudies-arrayexpress

Expression data from CD4+ naïve T cells under Treg-inducing condition in the presence or absence of butyrate

Project description:Commensal bacteria shape the gut immune system. Colonization bacteria increase the frequency of regulatory T cells, however, the molecular mechanisms are not yet known. To reveal the mechanism, we isolated naïve CD4+ T cells from the spleen of C57BL/6 mice and cultured the cells under Treg-inducing condition culture in the presence or absence of butyrate, a metabolite produced by commensal bacteria.

2015-06-12 | GSE48045 | GEO

Expression data from CD4+ naïve T cells under Treg-inducing condition in the presence or absence of butyrate

2015-06-12 | E-GEOD-48045 | biostudies-arrayexpress

Regulation of gene expression in IECs by HDAC3 under germ-free conditions

Project description:The development and severity of inflammatory bowel diseases (IBD) and other chronic inflammatory conditions can be influenced by host genetic and environmental factors, including signals derived from commensal bacteria. However, the mechanisms that integrate these diverse cues remain undefined. Here we demonstrate that intestinal epithelial cells (IECs) isolated from IBD patients exhibit decreased expression of the epigenome-modifying enzyme histone deacetylase 3 (HDAC3). Further, genome-wide analyses of murine IECs that lack HDAC3 (HDAC3ΔIEC) revealed that HDAC3 deficiency resulted in dysregulated gene expression coupled with alterations in histone acetylation. Critically, conventionally-housed HDAC3ΔIEC mice demonstrated loss of Paneth cells, impaired IEC function and alterations in the composition of intestinal commensal bacteria. In addition, HDAC3ΔIEC mice exhibited significantly increased susceptibility to intestinal damage and inflammation, indicating that epithelial expression of HDAC3 plays a central role in maintaining intestinal homeostasis. Strikingly, rederivation of HDAC3ΔIEC mice into germ-free conditions revealed that dysregulated IEC gene expression, Paneth cell homeostasis, and intestinal barrier function were largely restored in the absence of commensal bacteria. Collectively, these data indicate that the HDAC3 is a critical factor that integrates commensal bacteria-derived signals to calibrate epithelial cell responses required to establish normal host-commensal relationships and maintain intestinal homeostasis.

2013-11-12 | GSE50189 | GEO

Regulation of gene expression in IECs by HDAC3 under germ-free conditions

2013-11-12 | E-GEOD-50189 | biostudies-arrayexpress

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