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Effect of Bacteroides vulgatus on colitis and depressive-like behavior in a murine model of inflammatory bowel disease: involvement of the gut-brain axis

ABSTRACT: Effect of Bacteroides vulgatus on colitis and depressive-like behavior in a murine model of inflammatory bowel disease: involvement of the gut-brain axis

PROVIDER: PRJNA1031573 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26499745_1.fastq.gz	Fastqsanger.gz
	SRR26499745_2.fastq.gz	Fastqsanger.gz
	SRR26499746_1.fastq.gz	Fastqsanger.gz
	SRR26499746_2.fastq.gz	Fastqsanger.gz
	SRR26499747.fastq.gz	Fastqsanger.gz

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Effect of Bacteroides vulgatus on colitis and depressive-like behavior in a murine model of inflammatory bowel disease: involvement of the gut-brain axis

Project description:IBD is characterized by chronic recurrences of intestinal inflammation and intestinal immune disturbances.Bacteroides vulgatus can alleviate DSS-induced colitis in mice, but the mechanism is unknown. The aim of this study was to examine the changes in gene expression in the intestinal tissue of mice with colitis following treatment with Bacteroides vulgatus by RNA sequencing.

2023-12-06 | GSE246118 | GEO

Aberrant H3.3 dynamics in NAc promote vulnerability to depressive-like behavior

Project description:Human major depressive disorder (MDD), along with related mood disorders, is among the world’s greatest public health concerns, however, its pathophysiology remains poorly understood. Persistent changes in gene expression are known to promote physiological aberrations implicated in MDD. More recently, histone mechanisms affecting cell-type and regional specific chromatin structures have also been shown to contribute to transcriptional programs related to depressive behaviors, as well as responses to antidepressants (ADs). Although much emphasis has been placed in recent years on roles for histone posttranslational modifications (PTMs) and chromatin remodeling events in the etiology of MDD, it has become increasingly clear that replication-independent histone variants (e.g., H3.3), which differ in primary amino acid sequence from their canonical counterparts, similarly play critical roles in the regulation of activity-dependent neuronal transcription, synaptic connectivity and behavioral plasticity. Here, we demonstrate a novel role for increased H3.3 dynamics in nucleus accumbens (NAc)––a key limbic brain reward region––in the regulation of aberrant social stress-mediated gene expression, abnormal dendritic morphology and the precipitation of depressive-like behaviors in mice. We find that molecular blockade of these dynamics promotes resilience to chronic social stress and results in a partial re-normalization of stress-associated transcriptional patterns in NAc. In sum, our findings establish H3.3 dynamics as a critical, and previously undocumented, regulator of mood, and suggest that future therapies aimed at modulating striatal histone dynamics may potentiate beneficial behavioral adaptations to negative emotional stimuli.

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Repeated exposure with short-term behavioral stress resolves pre-existing stress-induced depressive-like behavior in mice

Project description:Chronic stress induces adaptive changes in the brain via the cumulative action of glucocorticoids, which is associated with mood disorders. Here we show that repeated daily five-minute restraint resolves pre-existing stress-induced depressive-like behavior in mice. Repeated injection of glucocorticoids in low doses mimics the anti-depressive effects of short-term stress. Repeated exposure to short-term stress and injection of glucocorticoids activate neurons in largely overlapping regions of the brain, as shown by c-Fos staining, and reverse distinct stress-induced gene expression profiles. Chemogenetic inhibition of neurons in the prelimbic cortex projecting to the nucleus accumbens, basolateral amygdala, or bed nucleus of the stria terminalis results in anti-depressive effects similarly to short-term stress exposure, while only inhibition of neurons in the prelimbic cortex projecting to the bed nucleus of the stria terminalis rescues glucocorticoid release. In summary, we show that short-term stress can reverse adaptively altered stress gains and resolve stress-induced depressive-like behavior.

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Antidepressants affect gut microbiota and Ruminococcus flavefaciens is able to abolish their effects on depressive-like behavior

Project description:Accumulating evidence demonstrates that the gut microbiota affects brain function and behavior, including depressive behavior. Antidepressants are the main drugs used for treatment of depression. We hypothesized that antidepressant treatment could modify gut microbiota which can partially mediate their antidepressant effects. Mice were chronically treated with one of five antidepressants (fluoxetine, escitalopram, venlafaxine, duloxetine or desipramine), and gut microbiota was analyzed, using 16s rRNA gene sequencing. After characterization of differences in the microbiota, chosen bacterial species were supplemented to vehicle and antidepressant-treated mice, and depressive-like behavior was assessed to determine bacterial effects. RNA-seq analysis was performed to determine effects of bacterial treatment in the brain. Antidepressants reduced richness and increased beta diversity of gut bacteria, compared to controls. At the genus level, antidepressants reduced abundances of Ruminococcus, Adlercreutzia, and an unclassified Alphaproteobacteria. To examine implications of the dysregulated bacteria, we chose one of antidepressants (duloxetine) and investigated if its antidepressive effects can be attenuated by simultaneous treatment with Ruminococcus flavefaciens or Adlercreutzia equolifaciens. Supplementation with R. flavefaciens diminished duloxetine-induced decrease in depressive-like behavior, while A. equolifaciens had no such effect. R. flavefaciens treatment induced changes in cortical gene expression, up-regulating genes involved in mitochondrial oxidative phosphorylation, while down-regulating genes involved in neuronal plasticity. Our results demonstrate that various types of antidepressants alter gut microbiota composition, and further implicate a role for R. flavefaciens in alleviating depressive-like behavior.

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