Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA126935 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Comparison of murine colonic mucosal gene expression between postanatal day 90 (P90) to postnatal day 30 (P30) by whole genomic expression microarray. Gene expression profiling of colonic mucosal DNA between P90 and P30 mice. Agilent Technologies two-color labelling kit and genomic hybridization protocol was utilized.
2010-01-30 | GSE19506 | GEO
Project description:BACKGROUND & AIMS: Toll-like receptor 2 (Tlr2) is important in bacterial pattern recognition and has been recognized as a modifier of intestinal inflammation. In this study we sought to determine the epigenomic, transcriptomic and microbiomic consequences of Tlr2 deficiency in the colonic mucosa of mice to gain insights into biological pathways that shape the interface between the gut microflora and the mammalian host. METHODS: Colonic mucosa from C57BL/6 and Tlr2-/- mice was interrogated by methylation specific amplification microarray (MSAM) to screen for changes in DNA methylation, with bisulfite pyrosequencing validation. Transcriptomic changes in the same tissue were analyzed by microarray expression profiling and real time RT-PCR. The mucosal microbiome was studied by high throughput, detailed pyrosequencing of 16S RNA. RESULTS: Tlr2 deficiency influenced the methylation of about 1% of the interrogated genome and resulted in a significant expression change in a similar percentage of all transcripts studied. Importantly, gene ontology analysis revealed that the expression of genes involved in immune processes is significantly modified by the absence of Tlr2, some of which have been already linked to inflammatory bowel diseases (Stat1, Anpep), for example. Overlaps between DNA methylation and gene expression changes were confirmed at Anpep and Ifit2. The epigenomic and transcriptomic modifications associated with alteration in mucosal microbial composition, affecting 11% of the detected bacterial species in the Tlr2-/- animals. CONCLUSIONS: Tlr2 deficiency induces colonic mucosal epigenomic, transcriptomic and microbiomic changes underscoring the intricate network of biological processes that provide the link between genotype and phenotype in mammals. Our findings bare implications for common gastrointestinal disorders such as IBD and colon cancer.
2010-07-01 | GSE21845 | GEO
Project description:Comparison of murine colonic mucosal DNA from postnatal day 90 (P90) to postnatal day 30 (P30) by MSAM
| PRJNA119269 | ENA
Project description:BACKGROUND & AIMS: Toll-like receptor 2 (Tlr2) is important in bacterial pattern recognition and has been recognized as a modifier of intestinal inflammation. In this study we sought to determine the epigenomic, transcriptomic and microbiomic consequences of Tlr2 deficiency in the colonic mucosa of mice to gain insights into biological pathways that shape the interface between the gut microflora and the mammalian host. METHODS: Colonic mucosa from C57BL/6 and Tlr2-/- mice was interrogated by methylation specific amplification microarray (MSAM) to screen for changes in DNA methylation, with bisulfite pyrosequencing validation. Transcriptomic changes in the same tissue were analyzed by microarray expression profiling and real time RT-PCR. The mucosal microbiome was studied by high throughput, detailed pyrosequencing of 16S RNA. RESULTS: Tlr2 deficiency influenced the methylation of about 1% of the interrogated genome and resulted in a significant expression change in a similar percentage of all transcripts studied. Importantly, gene ontology analysis revealed that the expression of genes involved in immune processes is significantly modified by the absence of Tlr2, some of which have been already linked to inflammatory bowel diseases (Stat1, Anpep), for example. Overlaps between DNA methylation and gene expression changes were confirmed at Anpep and Ifit2. The epigenomic and transcriptomic modifications associated with alteration in mucosal microbial composition, affecting 11% of the detected bacterial species in the Tlr2-/- animals. CONCLUSIONS: Tlr2 deficiency induces colonic mucosal epigenomic, transcriptomic and microbiomic changes underscoring the intricate network of biological processes that provide the link between genotype and phenotype in mammals. Our findings bare implications for common gastrointestinal disorders such as IBD and colon cancer. [MSAM]: Methylation profiling. Two independent Tlr2-/- to WT comparisons were performed as follows. Samples were labelled with Cy3 (WT) and Cy5 (Tlr2-/-) and two independent Tlr2-/- to WT comparisons were done on a 2x105k microarray containing probes, covering 33,404 (81% of all) SmaI intervals between 100 bp and 2.2 kb in the mouse genome. [mRNA]: mRNA profiling. 4 independent Tlr2-/- to WT comparisons were performed as follows. RNA (0.4ug) samples were processed and labelled with Cy3 and Cy5 (Quick Amp labelling kit, two color, Agilent technologies) and 4 independent Tlr2-/- to WT comparisons were done on Agilent technologies 4x44k whole genomic expression microarray G2519F, Amadid:014868). The Supplementary files below contain processed data from the MSAM and expression microarrays. For the MSAM: an interval was considered a 'hit' if the averaged probe ratios within an interval showed a >1.6 fold change in both Tlr2-/- vs. WT comparisons. For the expression microarrays: transcripts were considered a 'hit' if probe average intensities showed a >1.6 fold change in at least two microarray comparisons out of four, with the remaining arrays not contradicting the increase or decrease of expression (i.e.: 1 or above 1 in case at least two other >1.6; 1 or less than 1 in case at least two other <0.625).
2010-07-01 | E-GEOD-21845 | biostudies-arrayexpress
Project description:Comparison of murine colonic mucosal gene expression between postanatal day 90 (P90) to postnatal day 30 (P30)
| PRJNA122329 | ENA
Project description:DNA methylation profiling of colonic mucosal DNA between P90 and P30 mice. 0.5ug of DNA was serially digested with SmaI and XmaI followed by an adaptor ligation and adaptor mediated PCR amplification
2009-09-30 | GSE18031 | GEO
Project description:Transcriptional profiling of microscopically laser dissected murine colonic tissue from 3 separate normal crypts, wound associated epithelium (WAE), normal epithelium, and regenerating crypts (day 6 only) at days 2,4,and 6 after colonic mucosal injury. Injury model performed as described in: H. Seno et al., Efficient colonic mucosal wound repair requires Trem2 signaling. Proc. Natl. Acad. Sci. USA 106, 256-261 (2009)
2012-06-18 | E-MTAB-1175 | biostudies-arrayexpress
Project description:Leber2015 - Mucosal immunity and gut
microbiome interaction during C. difficile infection
This model is described in the article:
Systems Modeling of
Interactions between Mucosal Immunity and the Gut Microbiome
during Clostridium difficile Infection.
Leber A, Viladomiu M, Hontecillas R,
Abedi V, Philipson C, Hoops S, Howard B, Bassaganya-Riera
J.
PLoS ONE 2015; 10(7): e0134849
Abstract:
Clostridium difficile infections are associated with the use
of broad-spectrum antibiotics and result in an exuberant
inflammatory response, leading to nosocomial diarrhea, colitis
and even death. To better understand the dynamics of mucosal
immunity during C. difficile infection from initiation through
expansion to resolution, we built a computational model of the
mucosal immune response to the bacterium. The model was
calibrated using data from a mouse model of C. difficile
infection. The model demonstrates a crucial role of T helper 17
(Th17) effector responses in the colonic lamina propria and
luminal commensal bacteria populations in the clearance of C.
difficile and colonic pathology, whereas regulatory T (Treg)
cells responses are associated with the recovery phase. In
addition, the production of anti-microbial peptides by inflamed
epithelial cells and activated neutrophils in response to C.
difficile infection inhibit the re-growth of beneficial
commensal bacterial species. Computational simulations suggest
that the removal of neutrophil and epithelial cell derived
anti-microbial inhibitions, separately and together, on
commensal bacterial regrowth promote recovery and minimize
colonic inflammatory pathology. Simulation results predict a
decrease in colonic inflammatory markers, such as neutrophilic
influx and Th17 cells in the colonic lamina propria, and length
of infection with accelerated commensal bacteria re-growth
through altered anti-microbial inhibition. Computational
modeling provides novel insights on the therapeutic value of
repopulating the colonic microbiome and inducing regulatory
mucosal immune responses during C. difficile infection. Thus,
modeling mucosal immunity-gut microbiota interactions has the
potential to guide the development of targeted fecal
transplantation therapies in the context of precision medicine
interventions.
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2024-09-02 | BIOMD0000000583 | BioModels
Project description:Comparison of murine colonic mucosal gene expression between offspring born to mothers fed a methyl donor diet (MD) versus control at postnatal day 90 (P90).
| PRJNA132807 | ENA
Project description:Streptococcus suis is an emerging zoonotic agent causing meningitis and septicemia. Outbreaks in humans in China with atypical cases of streptococcal toxic shock-like syndrome have been described to be caused by a clonal epidemic S. suis strain characterized as sequence type (ST) 7 by multilocus sequence typing, different from the classical ST1 usually isolated in Europe. Previous in vitro studies showed that Toll-like receptor (TLR) 2 plays a major role in S. suis ST1 interactions with host cells. In the present study, the in vivo role of TLR2 in systemic infections caused by S. suis ST1 or ST7 strains using TLR2 deficient (TLR2-/-) mice was evaluated. TLR2-mediated recognition significantly contributes to the acute disease caused by the highly virulent S. suis ST1 strain, since the TLR2-/- mice remained unaffected when compared to wild type (WT) mice. The lack of mortality could not be associated with a lower bacterial burden; however, a significant decrease in the induction of pro-inflammatory mediators, as evaluated by microarray, real-time PCR and protein assays, was observed. On the other hand, TLR2-/- mice infected with the epidemic ST7 strain presented no significant differences regarding survival and expression of pro-inflammatory mediators when compared to the WT mice. Together, these results show a TLR2-independent host innate immune response to S. suis that depends on the strain. Total RNA obtained from spleen of C57BL/6 mice or C57BL/6 TLR2-KO mice infected with Streptococcus suis strain P1/7. Four replicates in both groups.
2013-06-01 | E-GEOD-45861 | biostudies-arrayexpress