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A synbiotic intervention modulates meta-omics signatures of gut redox potential and acidity in elective caesarean born infants

ABSTRACT: A synbiotic intervention modulates meta-omics signatures of gut redox potential and acidity in elective caesarean born infants

PROVIDER: PRJEB44790 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR5900050_1.fastq.gz	Fastqsanger.gz
	ERR5900050_2.fastq.gz	Fastqsanger.gz
	ERR5900060_1.fastq.gz	Fastqsanger.gz
	ERR5900060_2.fastq.gz	Fastqsanger.gz
	ERR5900560_1.fastq.gz	Fastqsanger.gz

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human metagenome

Project description:A synbiotic intervention modulates meta-omics signatures of gut redox potential and acidity in elective caesarean born infants

| PRJNA726032 | ENA

A synbiotic intervention modulates meta-omics signatures of gut redox potential and acidity in elective caesarean born infants.

Project description:BackgroundThe compromised gut microbiome that results from C-section birth has been hypothesized as a risk factor for the development of non-communicable diseases (NCD). In a double-blind randomized controlled study, 153 infants born by elective C-section received an infant formula supplemented with either synbiotic, prebiotics, or unsupplemented from birth until 4 months old. Vaginally born infants were included as a reference group. Stool samples were collected from day 3 till week 22. Multi-omics were deployed to investigate the impact of mode of delivery and nutrition on the development of the infant gut microbiome, and uncover putative biological mechanisms underlying the role of a compromised microbiome as a risk factor for NCD.ResultsAs early as day 3, infants born vaginally presented a hypoxic and acidic gut environment characterized by an enrichment of strict anaerobes (Bifidobacteriaceae). Infants born by C-section presented the hallmark of a compromised microbiome driven by an enrichment of Enterobacteriaceae. This was associated with meta-omics signatures characteristic of a microbiome adapted to a more oxygen-rich gut environment, enriched with genes associated with reactive oxygen species metabolism and lipopolysaccharide biosynthesis, and depleted in genes involved in the metabolism of milk carbohydrates. The synbiotic formula modulated expression of microbial genes involved in (oligo)saccharide metabolism, which emulates the eco-physiological gut environment observed in vaginally born infants. The resulting hypoxic and acidic milieu prevented the establishment of a compromised microbiome.ConclusionsThis study deciphers the putative functional hallmarks of a compromised microbiome acquired during C-section birth, and the impact of nutrition that may counteract disturbed microbiome development.Trial registrationThe study was registered in the Dutch Trial Register (Number: 2838 ) on 4th April 2011.

| S-EPMC8229302 | biostudies-literature

Synbiotic-Derived Metabolites Alleviate Stress-Induced Depression by Regulating Lymphocyte Activation through the Aryl Hydrocarbon Receptor

Project description:Synbiotics are a combination of probiotics and prebiotics which can alter the composition of the gastrointestinal tract evoking beneficial effects throughout the body through the production of a battery of bioactive metabolites. In this study, a synbiotic was used to reduce the behavioral and biochemical symptoms of depression and this nanostring panel was used to decipher where along the gut-brain-axis the synbiotic-derived metabolites were invoking their beneficial effects on the immune system. The synbitoic was composed of two probiotic bacteria (Lactobacillus fermentum ATCC 793 and Bifidobacteria longum ATCC 15707 and a grape -derived prebiotic composed of grape seed polyphenol extract, resveratrol and a concord grape extract. Male mice (C57BL/6) were pretreatment with either nothing (control), BDPP, probiotic or synbiotic and underwent 28 days of chronic unpredicitable stress. After 28 days, animals' behavior reflected an increase in depressive- and anxiety-like behavior, rescued specifically by the synbiotic. This nanostring multiplex analysis reveals both tissue- and treatment-specific effects on immune modulators.

2020-11-03 | GSE148579 | GEO

synbiotic probiotics

Project description:synbiotic probiotics Raw sequence reads

| PRJNA1119906 | ENA

Bacterial extracellular vesicles of human amniotic fluid and maternal feces

Project description:Fecal and amniotic fluid samples were collected from 25 pregnant women undergoing elective Caesarean section delivery after a term pregnancy at Oulu University Hospital, Oulu, Finland. Extracellular vesicles (EVs) were isolated from both sample types and their protein cargo analyzed using LC-ESI-MS/MS.

2023-11-14 | PXD045755 | Pride

Acidity-mediated induction of FoxP3+ regulatory T cells

Project description:Regulatory T cells (Tregs) are known to maintain survival and suppressive function in the presence of high levels of extracellular lactic acid. However, the effect of lactic acid on Treg induction is not known. We therfore evaluated the effect of lactic acid on Treg induction and observed an increased induction of Tregs in the presence of lactic acid. This increase occurred in a glycolysis-independent, acidity-dependent manner.

2023-03-23 | GSE217536 | GEO

Project description:Vaginal microbiota transfer in caesarean-born infants

| PRJNA930562 | ENA

Project description:Vaginal microbiota transfer in caesarean-born infants

| PRJNA945351 | ENA

Respiratory complex I controls persister formation through regulation of intracellular acidity and protein synthesis

Project description:Respiratory complex I controls persister formation through regulation of intracellular acidity and protein synthesis.

2022-01-13 | PXD029006 | Pride

Acidity perturbs IL-2 responsiveness, mTORC1 and c-Myc in CD8+ T cells

Project description:CD8+T cells play a critical role in tumor control but a range of barriers in the microenvironment including low pH can suppress their function.Here, we demonstrate that acidity dampens T-cell expansion mainly due to impaired IL-2 responsiveness, blunts cytokine secretion upon re-activation, and lowers the cytolytic capacity ofCD8+T cells expressing weak affinity TCR. We further reveal decreases in both mTORC1 signaling and c-Myc levels at low pH.Mechanistically, concomitantly to nuclear/cytoplasmic acidification, mTORC1 was disrupted in a Rheb-, Akt/TSC2/PRAS40-, GATOR1- and Lkb1/AMPK -independent manner, and c-Myc levels dropped due to both decreased transcription and higher proteasome-mediated degradation. In addition, lower intracellular levels of glutamine/glutamate/aspartate and elevated proline were observed with no apparent impact on mTORC1 or c-Myc. Overall, we conclude that, due to the broad disruption caused by acidity, multiple interventions will be required to restore T-cell function unless intracellular pH can be effectively restored.

2024-06-13 | GSE269681 | GEO

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