Microbiota-dependent gene expression in small intestinal epithelial cells (IECs)
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE35597 | GEO | 2012/05/17
SECONDARY ACCESSION(S): PRJNA152515
REPOSITORIES: GEO
Similar Datasets
Project description:Intestinal epithelial cells were isolated from total small intestine of each four 28-day old conventionally raised (conv) and germ-free (GF) bred C57BL/6 mice (protocol according to: Lotz et al., J. Exp Med. 2006). Total RNA was isolated by TriZol and ist purity was examined using a Bioanalyszer. We used microarrays to comparatively detail the global gene expression in primary total isolated intestinal epithelial cells. Four biological replicates from isolated intestinal epithelial cells obtained from each 4 germ-free bred and conventionally raised mice. Colour change.
2012-05-16 | E-GEOD-35597 | biostudies-arrayexpress
Project description:Intestinal epithelial cells were isolated from total small intestine of each four 3- and 21-day-old C57BL/6 mice (protocol according to: Lotz et al., J. Exp. Med. 2006). Each two 3- and 21-day-old animals were obtained from one litter. Total RNA was isolated by TriZol and ist purity was examined using a Bioanalyszer. We used microarrays to detail the global gene expression in primary total isolated intestinal epithelial cells of 3- versus 21-day-old mice.
2012-05-17 | GSE35596 | GEO
Project description:Intestinal epithelial cells were isolated from total small intestine of each four 3- and 21-day-old C57BL/6 mice (protocol according to: Lotz et al., J. Exp. Med. 2006). Each two 3- and 21-day-old animals were obtained from one litter. Total RNA was isolated by TriZol and ist purity was examined using a Bioanalyszer. We used microarrays to detail the global gene expression in primary total isolated intestinal epithelial cells of 3- versus 21-day-old mice. Four biological replicates from isolated intestinal epithelial cells obtained from 3- and 21-day-old mice (each two animals from one litter). Colour change.
2012-05-16 | E-GEOD-35596 | biostudies-arrayexpress
Project description:Intestinal epithelial cells of 28-day-old female mice were isolated according to a recently published protocol (Lotz et al., J Exp. Med. 2006).
2014-08-23 | GSE51269 | GEO
Project description:1-day-old C57BL/6 mice were left untreated (co) or orally infected with 10E2 CFU wildtype (wt) or delta invC SPI1 mutant Salmonella Typhimurium (ATCC14028). Four biological replicates obtained from individual animals were exmained; each group contained animals from at least 2 different litters. On day 4 p.i., animals were sacrificed and intestinal epithelial cells were isolated from total small intestine (protocol according to: Lotz et al., J. Exp. Med. 2006). Total RNA was isolated by TriZol and its purity was examined using a Bioanalyzer. We used microarrays to detail the global gene expression in primary total isolated intestinal epithelial cells.
2014-09-01 | GSE51160 | GEO
Project description:Intestinal epithelial cells of 28-day-old female mice were isolated according to a recently published protocol (Lotz et al., J Exp. Med. 2006). Isolated intestinal epithelial cells of four individual animals (four biological replicates) were examined. Single color array.
2014-08-23 | E-GEOD-51269 | biostudies-arrayexpress
Project description:1-day-old C57BL/6 mice were left untreated (co) or orally infected with 10E2 CFU wildtype (wt) or delta invC SPI1 mutant Salmonella Typhimurium (ATCC14028). Four biological replicates obtained from individual animals were exmained; each group contained animals from at least 2 different litters. On day 4 p.i., animals were sacrificed and intestinal epithelial cells were isolated from total small intestine (protocol according to: Lotz et al., J. Exp. Med. 2006). Total RNA was isolated by TriZol and its purity was examined using a Bioanalyzer. We used microarrays to detail the global gene expression in primary total isolated intestinal epithelial cells. Four biological replicates of isolated intestinal epithelial cells obtained 4 daysp.i. from neonate mice infected at the age of 1 day (each group with animals from at least two litteres). Single color array.
2014-09-01 | E-GEOD-51160 | biostudies-arrayexpress
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. Analyses of histone acetylation in primary IECs from HDAC3FF (3 biologic replicates) and HDAC3ΔIEC (3 biologic replicates) mice were conducted utilizing ChIP-seq for H3K9Ac.
2013-12-02 | E-GEOD-50453 | biostudies-arrayexpress
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 | GSE50188 | GEO
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.
2013-12-02 | GSE50453 | GEO