Mouse gut microbes
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ABSTRACT:
PROVIDER: PRJNA633670 | ENA |
REPOSITORIES: ENA
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Project description:Gut-brain connections monitor the intestinal tissue and its microbial and dietary content1, regulating both intestinal physiological functions such as nutrient absorption and motility2,3, and brain–wired feeding behaviour2. It is therefore plausible that circuits exist to detect gut microbes and relay this information to central nervous system (CNS) areas that, in turn, regulate gut physiology4. We characterized the influence of the microbiota on enteric–associated neurons (EAN) by combining gnotobiotic mouse models with transcriptomics, circuit–tracing methods, and functional manipulation. We found that the gut microbiome modulates gut–extrinsic sympathetic neurons; while microbiota depletion led to increased cFos expression, colonization of germ-free mice with short-chain fatty acid–producing bacteria suppressed cFos expression in the gut sympathetic ganglia. Chemogenetic manipulations, translational profiling, and anterograde tracing identified a subset of distal intestine-projecting vagal neurons positioned to play an afferent role in microbiota–mediated modulation of gut sympathetic neurons. Retrograde polysynaptic neuronal tracing from the intestinal wall identified brainstem sensory nuclei activated during microbial depletion, as well as efferent sympathetic premotor glutamatergic neurons that regulate gastrointestinal transit. These results reveal microbiota–dependent control of gut extrinsic sympathetic activation through a gut-brain circuit.
2020-03-20 | GSE145986 | GEO
Project description:We report the application of bulk RNA-sequencing-based technology for high-throughput profiling to examine the individual and combinatorial effects of the liver circadian clock and gut microbes on the liver transcriptome over 24-hours. Principle Component Analysis demonstrated that functionality of the liver circadian clock is the primary driver of the hepatic transcriptome profile, and presence of microbes is the secondary driver. We identified a range of significantly oscillating transcripts within each experimental group using empirical_JTK_CYCLE, and revealed an overall increase in oscillating transcripts with both the loss of cuntional liver clock and gut microbes. Network analysis via Spearman correlation revealed that a broken liver clock results in increased connections and correlated transcripts only in the presence of gut microbes. Finally, we show by differential expression and gene set enrichment analysis that several key metabolic pathways, particularly carbohydrate and lipid metabolism, were significantly downregulated when the liver clock is broken, regardless of microbial status. This study demonstrates the complex contributions of the liver circadian clock and gut microbes in transcriptome programming, both over time and overall.
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Project description:This study examines the role of early exposure to gut microbes and poor diet on microglial function in mice. Groups = control (CON), malnourished (MAL), and malnourished + microbial exposure (E/MALBG). CD11b+ cells (microglial enrichment) were isolated from whole mouse brains (Adult Brain Disruption Kit, Miltenyi Biotec). After sample quality control (Agilent 2100 Bioanalyzer), qualifying samples were sent for RNA-Seq (Illumina NextSeq 500 with Paired End 42bp × 42bp reads; demultiplexed: Illumina's bcl2fastq2). Following alignment against mouse reference genes (STAR aligner), DEG analyses was conducted using the DESeq2 pipeline.
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