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Dysbacteriosis-induced LPS elevation disturbs the development of muscle progenitor cells by interfering with retinoic acid signaling [RNA-seq]

ABSTRACT: Whether myogenesis is affected by the maternal gut dysbacteriosis still remains ambiguous. In this study, firstly we show elevated level of lipopolysaccharides (LPS) in a gut microbiota dysbiosis mouse model. Secondly, we demonstrate that the diameter of muscle fibres, limb development and somitogenesis were inhibited in both gut microbiota dysbiosis and LPS exposed mice and chicken embryos. These might be due to LPS disturbed the cell survival and the key genes which regulating the somitogenesis and myogenesis. RNA sequencing and subsequent validation experiments verified that retinoic acid (RA) signaling perturbation was mainly responsible for the aberrant somite formation and differentiation. Subsequently, we found that LPS-induced Roxidative stress (ROS generation and antioxidant genes such as Nrf2, AKR) contributed to the above-mentioned interference with RA signaling. These findings highlight that the gut microbiota homeostasis also involved in regulating the development of muscle progenitor cells during pregnancy.

ORGANISM(S): Gallus gallus

PROVIDER: GSE139525 | GEO | 2020/05/08

REPOSITORIES: GEO

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Dysbacteriosis-induced LPS elevation disturbs the development of muscle progenitor cells by interfering with retinoic acid signaling [16S rRNA sequencing]

Project description:Whether myogenesis is affected by the maternal gut dysbacteriosis still remains ambiguous. In this study, firstly we show elevated level of lipopolysaccharides (LPS) in a gut microbiota dysbiosis mouse model. Secondly, we demonstrate that the diameter of muscle fibres, limb development and somitogenesis were inhibited in both gut microbiota dysbiosis and LPS exposed mice and chicken embryos. These might be due to LPS disturbed the cell survival and the key genes which regulating the somitogenesis and myogenesis. RNA sequencing and subsequent validation experiments verified that retinoic acid (RA) signaling perturbation was mainly responsible for the aberrant somite formation and differentiation. Subsequently, we found that LPS-induced Roxidative stress (ROS generation and antioxidant genes such as Nrf2, AKR) contributed to the above-mentioned interference with RA signaling. These findings highlight that the gut microbiota homeostasis also involved in regulating the development of muscle progenitor cells during pregnancy.

2020-05-08 | GSE139422 | GEO

DNA methylation profiles of mouse sperm in response to antibiotic-induced gut microbiota dysbiosis using whole-genome bisulfite sequencing

Project description:DNA methylation profile of mouse sperm from conventionally-raised mice and gut dysbiosis experienced mice were characterized using whole-genome bisulfite sequencing. Genome-wide DNA methylation changes between control and dysbiotic male�s sperm were highly comparable, with no change in DNAme globally or at genomic features, only 21 differentially methylated regions (DMR) were identified, which did not overlap known regulatory elements. Epididymal sperm samples were harvested from 11 weeks old inbred male mice that were experiencing gut microbiota dysbiosis for 6-week (antibiotics treated, n=5), or drink sterilized water (control, n=5).

2023-11-13 | E-MTAB-10033 | biostudies-arrayexpress

Functional characterization of inflammatory bowel disease-associated gut dysbiosis in gnotobiotic mice

Project description:Gut dysbiosis is closely involved in the pathogenesis of inflammatory bowel disease (IBD). However, it remains unclear whether IBD-associated gut dysbiosis plays a primary role in disease manifestation or is merely secondary to intestinal inflammation. Here, we established a humanized gnotobiotic (hGB) mouse system to assess the functional role of gut dysbiosis associated with two types of IBD - Crohn's disease (CD) and ulcerative colitis (UC). In order to explore the functional impact of dysbiotic microbiota in IBD patients on host immune responses, we analyzed gene expression profiles in colonic mucosa of hGB mice colonized with healty (HC), CD, and UC microbiota.

2015-10-10 | GSE73882 | GEO

Higher colonic proliferation and tumor prevalence amongst azoxymethane treated A/J mice receiving fecal microbiota transplants from old mice compared to recipients of young mice [16S rRNA-Seq]

Project description:Gut microbial dysbiosis can play a causal role of in colorectal cancer. Gut microbiota chnages with age and becomes moer pro-inflammatory. We sought to determine whether microbiota from Old donors promotes more tumor formation in recipients than meterial from young donors.

2023-11-30 | GSE237336 | GEO

Higher colonic proliferation and tumor prevalence amongst azoxymethane treated A/J mice receiving fecal microbiota transplants from old mice compared to recipients of young mice [RNA-Seq]

2023-11-30 | GSE237335 | GEO

Gut microbiota transplantation in conventional mice

Project description:Gut microbiota dysbiosis characterizes systemic metabolic alteration, yet its causality is debated. To address this issue, we transplanted antibiotic-free conventional wild-type mice with either dysbiotic (“obese”) or eubiotic (“lean”) gut microbiota and fed them either a NC or a 72%HFD. We report that, on NC, obese gut microbiota transplantation reduces hepatic gluconeogenesis with decreased hepatic PEPCK activity, compared to non-transplanted mice. Of note, this phenotype is blunted in conventional NOD2KO mice. By contrast, lean microbiota transplantation did not affect hepatic gluconeogenesis. In addition, obese microbiota transplantation changed both gut microbiota and microbiome of recipient mice. Interestingly, hepatic gluconeogenesis, PEPCK and G6Pase activity were reduced even once mice transplanted with the obese gut microbiota were fed a 72%HFD, together with reduced fed glycaemia and adiposity compared to non-transplanted mice. Notably, changes in gut microbiota and microbiome induced by the transplantation were still detectable on 72%HFD. Finally, we report that obese gut microbiota transplantation may impact on hepatic metabolism and even prevent HFD-increased hepatic gluconeogenesis. Our findings may provide a new vision of gut microbiota dysbiosis, useful for a better understanding of the aetiology of metabolic diseases. all livers are from NC-fed mice only.

2017-03-16 | GSE81318 | GEO

Gut microbiota rewires host mRNA m6A epitranscriptomic landscape via bile acid metabolism

Project description:Gut microbiota and their metabolites influence host gene expression and physiological status through diverse mechanisms. Here we investigate how gut microbiota and their metabolites impact host's mRNA m6A epitranscriptome in various antibiotic-induced microbiota dysbiosis models. With multi-omics analysis, we find that the imbalance of gut microbiota can rewire host mRNA m6A epitranscriptomic profiles in brain, liver and intestine. We further explore the underlying mechanisms regulating host mRNA m6A methylome by depleting the microbiota with ampicillin. Metabolomic profiling shows that cholic acids are the main down-regulated metabolites with Firmicutes as the most significantly reduced genus in ampicillin-treated mice comparing to untreated mice. Fecal microbiota transplantations in germ-free mice and metabolites supplementations in cells verify that cholic acids are associated with host mRNA m6A epitranscriptomic rewiring. Collectively, this study employs an integrative multi-omics analysis to demonstrate the impact of gut microbiota dysbiosis on host mRNA m6A epitranscriptomic landscape via cholic acid metabolism.

2024-04-21 | GSE218001 | GEO

Gut microbiota dysbiosis rewires host mRNA m6A epitranscriptomic landscape via bile acid metabolism

Project description:Gut microbiota and their metabolites influence host gene expression and physiological status through diverse mechanisms. Here we investigate how gut microbiota and their metabolites impact host′s mRNA m6A epitranscriptome in various antibiotic-induced microbiota dysbiosis models. With multi-omics analysis, we find that the imbalance of gut microbiota can rewire host mRNA m6A epitranscriptomic profiles in brain, liver and intestine. We further explore the underlying mechanisms regulating host mRNA m6A methylome by depleting the microbiota with ampicillin. Metabolomic profiling shows that cholic acids are the main down-regulated metabolites with Firmicutes as the most significantly reduced genus in ampicillin-treated mice comparing to untreated mice. Fecal microbiota transplantations in germ-free mice and metabolites supplementations in cells verify that cholic acids are associated with host mRNA m6A epitranscriptomic rewiring. Collectively, this study employs an integrative multi-omics analysis to demonstrate the impact of gut microbiota dysbiosis on host mRNA m6A epitranscriptomic landscape via cholic acid metabolism.

2024-04-21 | GSE216620 | GEO

Consequences of collagen induced inflammatory arthritis on circadian regulation of the gut microbiome.

Project description:Autoimmune diseases, such as rheumatoid arthritis, are associated with significant gut microbiota dysbiosis. Here we show that remodelling of 24h rhythms within the gut during inflammatory joint disease drives profound changes in the microbiome and gut permeability.

2023-03-15 | GSE184233 | GEO

Metaproteomic Monitoring of Perinatal Mouse Gut Microbiota

Project description:In the presented study, in order to unravel gut microbial community multiplicity and the influence of maternal milk nutrients (i.e., IgA) on gut mucosal microbiota onset and shaping, a mouse GM (MGM) was used as newborn study model to discuss genetic background and feeding modulation on gut microbiota in term of symbiosis, dysbiosis and rebiosis maintenance during early gut microbiota onset and programming after birth. Particularly, a bottom-up shotgun metaproteomic approach, combined with a computational pipeline, has been compred with a culturomics analysis of mouse gut microbiota, obtained by MALDI-TOF mass spectrometry (MS).

2016-10-13 | PXD004033 | Pride

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