Similar Datasets
Project description:Weaning diet switch brings gut microbiome maturation along with postnatal formation of sufficient matured β-cell mass. The matured gut microbiota elevated agonistic components of bile acid (BA) pool towards farnesoid X receptor (FXR) that was paralleling with the declined β-cell FXR expression. To investigate whether BA/FXR could link postnatal β-cell development and gut microbiota maturation, we forced persistent FXR expression in β cells (βFxrKI) and found decreased neonatal β-cell mass growth and increased glycemia in weaned βFxrKI mice, which could be partially recovered by ablating gut microbiota before weaning. scRNA and scATAC seq analysis showed different β cell growth trajectories with suppressed intrinsic cell proliferation and elevated cell apoptosis in βFxrKI. Caspase-6 was then identified as a dominant β-cell FXR downstream effector to mediate its regulation. The negative regulation of the FXR-Casp6 axis on postnatal β-cell mass expansion reflected a programmed cellular response to gut microbiota maturation in neonatal mice.
2025-11-13 | GSE241406 | GEO
Project description:Weaning diet switch brings gut microbiome maturation along with postnatal formation of sufficient matured β-cell mass. The matured gut microbiota elevated agonistic components of bile acid (BA) pool towards farnesoid X receptor (FXR) that was paralleling with the declined β-cell FXR expression. To investigate whether BA/FXR could link postnatal β-cell development and gut microbiota maturation, we forced persistent FXR expression in β cells (βFxrKI) and found decreased neonatal β-cell mass growth and increased glycemia in weaned βFxrKI mice, which could be partially recovered by ablating gut microbiota before weaning. scRNA and scATAC seq analysis showed different β cell growth trajectories with suppressed intrinsic cell proliferation and elevated cell apoptosis in βFxrKI. Caspase-6 was then identified as a dominant β-cell FXR downstream effector to mediate its regulation. The negative regulation of the FXR-Casp6 axis on postnatal β-cell mass expansion reflected a programmed cellular response to gut microbiota maturation in neonatal mice.
2025-11-13 | GSE241407 | GEO
Project description:Colonizing commensal bacteria after birth are required for the proper development of the gastrointestinal tract. It is believed that bacterial colonization pattern in neonatal gut affects gut barrier function and immune system maturation. Studies on the development of faecal flora microbiota in infants on various formula feeds showed that the neonatal gut was first colonized with enterococci followed by other flora microbiota such as Bifidobacterium in breast feeding infants. Intriguingly, Bjorksten group Other studies showed that Bbabies who developed allergy were less often colonized with Enterococcus during the first month of life as compared to healthy infants. A lot of Many studies have been done on conducted to elucidate how bifidobacteria or lactobacilli, some of which are considered probiotic, regulate infant gut immunity. However, much fewer studies have been focused on enterococi. In our study, we demonstrate that E. faecalis, isolated from healthy newborns, suppress inflammatory responses activated in vivo and in vitro. We found E. faecalis attenuates proinflammatory cytokine secretions, especially IL-8, through JNK and p38 signaling pathways. This finding shed light on how the first colonizer, E.faecalis, regulate inflammatory responses in the host. Samples are analysed using web-based GEArray Expression Analysis Suite
2014-04-04 | E-GEOD-56485 | biostudies-arrayexpress
Project description:The gut microbiota promotes immune system development in early life, but the interactions between the gut metabolome and immune cells in the neonatal gut remains largely undefined. Here, we demonstrate that the neonatal gut is uniquely enriched with neurotransmitters, including serotonin; specific gut bacteria produce serotonin directly while downregulating monoamine oxidase A to limit serotonin breakdown. Serotonin directly signals to T cells to increase intracellular indole-3-acetaldehdye to inhibit mTOR activation and thereby promotes the differentiation of regulatory T cells, both ex vivo and in vivo in the neonatal intestine. Oral gavage of serotonin into neonatal mice leads to long-term T cell-mediated antigen-specific immune tolerance towards both dietary antigens and commensal bacteria. Together, our study has uncovered an important role for unique gut bacteria to increase serotonin availability in the neonatal gut and a novel function of gut serotonin to shape T cell response to dietary antigens and commensal bacteria to promote immune tolerance in early life.
2024-01-31 | GSE248692 | GEO
Project description:The gut microbiota promotes immune system development in early life, but the interactions between the gut metabolome and immune cells in the neonatal gut remains largely undefined. Here, we demonstrate that the neonatal gut is uniquely enriched with neurotransmitters, including serotonin; specific gut bacteria produce serotonin directly while downregulating monoamine oxidase A to limit serotonin breakdown. Serotonin directly signals to T cells to increase intracellular indole-3-acetaldehdye to inhibit mTOR activation and thereby promotes the differentiation of regulatory T cells, both ex vivo and in vivo in the neonatal intestine. Oral gavage of serotonin into neonatal mice leads to long-term T cell-mediated antigen-specific immune tolerance towards both dietary antigens and commensal bacteria. Together, our study has uncovered an important role for unique gut bacteria to increase serotonin availability in the neonatal gut and a novel function of gut serotonin to shape T cell response to dietary antigens and commensal bacteria to promote immune tolerance in early life.
2024-01-31 | GSE248691 | GEO
Project description:The gut microbiota promotes immune system development in early life, but the interactions between the gut metabolome and immune cells in the neonatal gut remains largely undefined. Here, we demonstrate that the neonatal gut is uniquely enriched with neurotransmitters, including serotonin; specific gut bacteria produce serotonin directly while downregulating monoamine oxidase A to limit serotonin breakdown. Serotonin directly signals to T cells to increase intracellular indole-3-acetaldehdye to inhibit mTOR activation and thereby promotes the differentiation of regulatory T cells, both ex vivo and in vivo in the neonatal intestine. Oral gavage of serotonin into neonatal mice leads to long-term T cell-mediated antigen-specific immune tolerance towards both dietary antigens and commensal bacteria. Together, our study has uncovered an important role for unique gut bacteria to increase serotonin availability in the neonatal gut and a novel function of gut serotonin to shape T cell response to dietary antigens and commensal bacteria to promote immune tolerance in early life.
2024-01-31 | GSE248690 | GEO
Project description:An early settlement of a complex gut microbiota can protect against gastro-intestinal dysbiosis, but the effects of neonatal microbiota colonization on the gut barrier upon the further encounter of favorable bacteria or not, are largely unknown. The jejunal transcriptome of differently perfused intestinal loops of 12 caesarian-derived pigs previously associated with microbiota of different complexity was studied. Pigs received pasteurized sow colostrum at birth (d0), 2 mL of starter microbiota (10^7 CFU of each Lactob. Amylovorus (LAM), Clostr. glycolicum, and Parabacteroides spp.) on d1-d3 of age and either a placebo inoculant (simple association, SA) or an inoculant consisting of diluted feces of an adult sow (complex association, CA) on d3-d4 of age. On days 26-37 of age, jejunal loops were perfused for 8 h with either enterotoxigenic E. coli F4 (ETEC), F4 fimbriae (F4), LAM or saline (CTRL) and jejunal samples were obtained from each piglet immediately afterwards. The analysis of whole mRNA transcript expression was done by Affymetrix©Porcine Gene 1.1 ST array strips, a Robust Multichip Analysis was performed on the CEL files, and Transcripts IDâs were associated to 13,406 Human gene names, based on Sus scrofa Ensemble
2016-02-11 | E-GEOD-77787 | biostudies-arrayexpress
Project description:Asthma is the most prevalent chronic childhood disease in developed nations, yet its etiology remains incompletely understood. Emerging evidence suggest a crucial role for the gut microbiota in shaping immune development and future susceptibility to atopic disease. We previously demonstrated that short-chain fatty acids (SCFAs) as fermentation products of normal gut bacteria, regulate an innate type 2 immune axis that serves to dampen susceptibility to allergic lung inflammation. Here, we show that neonatal depletion of SCFA-producing gut bacteria via antibiotics robustly alters Lin⁻Sca-1⁺c-Kit⁺ (LSK) hematopoietic stem and progenitor cell (HSPC) output, resulting in a transplantable atopic immune phenotype: bone marrow (BM) transplants from these mice generates recipients with increased lung B cell IgE expression, elevated serum levels of IgE, dowstream increased IgE bound to basophils and exacerbated allergic lung inflammation following papain challenge. Notably, neonatal depletion of SCFA bacteria also enhanced susceptibility to chemotherapy (5-fluorocuracil) -induced myelosuppression, marked by impaired neutrophil recovery and increased DNA damage in long-term HSCs. Importantly, these antibiotic effects were reversed by supplementation of antibiotic-treated mice with exogenous SCFA. Single-cell RNA sequencing (scRNA-seq) of LSK HSPCs revealed distinct shifts in gene expression following vancomycin treatment, including increased proliferation-associated signatures with stress-adaptive features. Epigenetic profiling further revealed differential histone acetylation in HSPCs, consistent with an SCFA-mediated epigenetic regulatory mechanism. Collectively, these findings establish an epigenetic link between gut microbiota composition, hematopoiesis, and long-term immune function, providing a mechanistic basis for microbiota-driven atopic disease susceptibility and hematopoietic dysfunction.
2025-12-07 | GSE312386 | GEO
Project description:We have previously demonstrated that the gut microbiota can play a role in the pathogenesis of conditions associated with exposure to environmental pollutants. It is well accepted that diets high in fermentable fibers such as inulin can beneficially modulate the gut microbiota and lessen the severity of pro-inflammatory diseases. Therefore, we aimed to test the hypothesis that hyperlipidemic mice fed a diet enriched with inulin would be protected from the pro-inflammatory toxic effects of PCB 126.
2020-02-27 | E-MTAB-8798 | biostudies-arrayexpress
Project description:Colonizing commensal bacteria after birth are required for the proper development of the gastrointestinal tract. It is believed that bacterial colonization pattern in neonatal gut affects gut barrier function and immune system maturation. Studies on the development of faecal flora microbiota in infants on various formula feeds showed that the neonatal gut was first colonized with enterococci followed by other flora microbiota such as Bifidobacterium in breast feeding infants. Intriguingly, Bjorksten group Other studies showed that Bbabies who developed allergy were less often colonized with Enterococcus during the first month of life as compared to healthy infants. A lot of Many studies have been done on conducted to elucidate how bifidobacteria or lactobacilli, some of which are considered probiotic, regulate infant gut immunity. However, much fewer studies have been focused on enterococi. In our study, we demonstrate that E. faecalis, isolated from healthy newborns, suppress inflammatory responses activated in vivo and in vitro. We found E. faecalis attenuates proinflammatory cytokine secretions, especially IL-8, through JNK and p38 signaling pathways. This finding shed light on how the first colonizer, E.faecalis, regulate inflammatory responses in the host.
2014-04-04 | GSE56485 | GEO