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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

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: GSE47818 | GEO | 2015/06/10

SECONDARY ACCESSION(S): PRJNA208013

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

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 (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 (by Cd4Cre-Uhrf1flox/flox)

2014-04-07 | GSE56542 | 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

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. In this study, we performed gene expression profiling to examine how the transcriptional profiles in primary live, EpCAM+ IECs from the large intestine differed between germ-free control HDAC3FF mice (3 biological replicates) and germ-free IEC-intrinsic knockout HDAC3ΔIEC mice (3 biological replicates).

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

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

2013-11-12 | GSE50189 | GEO

Variability of gene expression profiles in neutrophils from Germ-free mice

Project description:Neutrophils, key cells of the innate immune system, are responsible for preventing bacterial infections. It was already demonstrated that albeit neutrophils synthesize lower levels of protein and RNA they are able to marked change its gene expression after bacteria exposure. The absence of microbial stimulation has consequences on development of the mucosal immune system as demonstrated using germ-free mice as a model. We are interested in understanding if commensal flora induces changes in the gene expression profile of neutrophils in its site of production, the bone marrow. Total RNA obtained from isolated neutrophils from Bone Marrow from Germ-free mice and control

2013-03-30 | E-GEOD-43511 | biostudies-arrayexpress

Expression data from germ free (GF) and specific pathogen free (SPF) mouse wound bed

Project description:Environmental factors that enhance regeneration are largely unknown. We hypothesized that skin bacteria modulate regeneration. Here, we assessed low, medium, and high levels of bacterial burden in Wound Induced Hair follicle Neogenesis (WIHN), a rare adult organogenesis model. WIHN levels and stem cell markers indeed correlated with bacterial counts, being lowest in germ free (GF), intermediate in conventional specific pathogen free (SPF), and highest even in mice infected with pathogenic Staphylococcus aureus. We identified IL-1β and keratinocyte-dependent IL-1R-MyD88 signaling as necessary and sufficient for bacteria to promote regeneration. Finally, in a small clinical trial, we found that a topical broad-spectrum antibiotic slowed skin wound healing. These results counter conventional notions that infection inhibits regeneration and the need for full sterility of small wounds.

2021-04-01 | GSE158613 | GEO

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