Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13007700_1.fastq.gz | Fastqsanger.gz | |||
| SRR13007700_2.fastq.gz | Fastqsanger.gz | |||
| SRR13007701_1.fastq.gz | Fastqsanger.gz | |||
| SRR13007701_2.fastq.gz | Fastqsanger.gz | |||
| SRR13007702_1.fastq.gz | Fastqsanger.gz |
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Project description:Newborn screening blood spots were obtained for neonates born to women enrolled in the Emory University African American Microbiome in Pregnacy Cohort
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Project description:In our model the newborns of asthmatic mother mice or of mothers exposed to air pollutant particles are born with a predisposition to asthma. Gut microbiome of these pups is altered, and the transplant of the pups’ microbiome (GMT) has conferred the asthma predisposition to naïve recipients. We hypothesized that bacteria alter metabolomic profile in the gut, which polarizes the dendritic cells (DC) in the recipient by affecting epigenetic regulation in these key decision-maker cells. Here we examined DNA methylation profiles in the recipient host’s DCs to test the prediction that GMT confers alterations in DNA methylation (not seen with sterilized GMT).
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Project description:Recent studies have unveiled the deep sea as a rich biosphere, populated by species descended from shallow-water ancestors post-mass extinctions. Research on genomic evolution and microbial symbiosis has shed light on how these species thrive in extreme deep-sea conditions. However, early adaptation stages, particularly the roles of conserved genes and symbiotic microbes, remain inadequately understood. This study examined transcriptomic and microbiome changes in shallow-water mussels Mytilus galloprovincialis exposed to deep-sea conditions at the Site-F cold seep in the South China Sea. Results reveal complex gene expression adjustments in stress response, immune defense, homeostasis, and energy metabolism pathways during adaptation. After 10 days of deep-sea exposure, shallow-water mussels and their microbial communities closely resembled those of native deep-sea mussels, demonstrating host and microbiome convergence in response to adaptive shifts. Notably, methanotrophic bacteria, key symbionts in native deep-sea mussels, emerged as a dominant group in the exposed mussels. Host genes involved in immune recognition and endocytosis correlated significantly with the abundance of these bacteria. Overall, our analyses provide insights into adaptive transcriptional regulation and microbiome dynamics of mussels in deep-sea environments, highlighting the roles of conserved genes and microbial community shifts in adapting to extreme environments.
2024-11-24 | GSE263620 | GEO
Project description:We explore whether a low-energy diet intervention for Metabolic dysfunction-associated steatohepatitis (MASH) improves liver disease by means of modulating the gut microbiome. 16 individuals were given a low-energy diet (880 kcal, consisting of bars, soups, and shakes) for 12 weeks, followed by a stepped re-introduction to whole for an additional 12 weeks. Stool samples were obtained at 0, 12, and 24 weeks for microbiome analysis. Fecal microbiome were measured using 16S rRNA gene sequencing. Positive control (Zymo DNA standard D6305) and negative control (PBS extraction) were included in the sequencing. We found that low-energy diet improved MASH disease without lasting alterations to the gut microbiome.
2024-12-31 | E-MTAB-14061 | biostudies-arrayexpress
Project description:To characterize the mitochondrial stress response induced by Doxycycline in vivo in liver and kidneys, we administered doxycycline (Dox) at 500 mg/kg/day (mpkd) in the drinking water to 9 weeks-old germ-free C57BL/6J mice for 16 days, hence eliminating the potential confounding impacts of Doxycycline on the microbiome.
2022-09-14 | GSE202754 | GEO
Project description:Maternal obesity impacts neonatal outcomes; however, its influence on fetal gene expression and early gut microbiota composition remains insufficiently characterized. This prospective study was conducted in 62 full-term neonates between 2022 and 2024, analyzing transcriptomic profiles from umbilical-cord blood and metagenomic sequencing of fecal samples at 4 months. The cohort included 31 neonates born to mothers with normal BMI (NBMI) and 31 neonates born to mothers with overweight or obesity (OBMI). Major congenital anomalies, maternal exposure to drugs or antibiotics were exclusion criteria. OBMI neonates demonstrated significant upregulation of genes related to inflammation (MPO, OLR1) and cell-cycle dysregulation (GADD45G, CCNA1). Evidence of altered lysosomal function was observed, with increased expression of CTSG and CLTCL1 and reduced expression of HYAL1. Microbiome analysis revealed a decrease in Bacteroidota and an increase in Proteobacteria in cesarean-delivered neonates. Holdemanella was enriched in vaginally delivered OBMI neonates, suggesting a potential adaptive microbial response. Enrichment of opportunistic pathogens, including Klebsiella, Morganella, and Enterococcus, was observed in cesarean-delivered neonates, indicating a combined effect of maternal obesity and delivery mode on early microbial colonization. These findings suggest that maternal obesity modifies neonatal immune and metabolic gene expression while reshaping gut microbiome composition, with potential implications for long-term health.
2026-07-29 | GSE303891 | GEO
Project description:Early life exposure to antibiotics alters the gut microbiome. These alterations lead to changes in metabolic homeostasis and an increase in host adiposity. We used microarrays to identify metabolic genes that may be up- or down-regulated secondary to antibiotic exposure. Low dose antibiotics have been widely used as growth promoters in the agricultural industry since the 1950’s, yet the mechanisms for this effect are unclear. Because antimicrobial agents of different classes and varying activity are effective across several vertebrate species, we hypothesized that such subtherapeutic administration alters the population structure of the gut microbiome as well as its metabolic capabilities. We generated a model of adiposity by giving subtherapeutic antibiotic therapy (STAT) to young mice and evaluated changes in the composition and capabilities of the gut microbiome. STAT administration increased adiposity in young mice and altered hormones related to metabolism. We observed substantial taxonomic changes in the microbiome, changes in copies of key genes involved in the metabolism of carbohydrates to short-chain fatty acids (SCFA), increases in colonic SCFA levels, and alterations in the regulation of hepatic metabolism of lipids and cholesterol. In this model, we demonstrate the alteration of early life murine metabolic homeostasis through antibiotic manipulation. C57BL6 mice were divided into low-dose penicillin or control groups. Given antibiotics via drinking water after weaning. Sacrificed and liver sections collected for RNA extraction.
2012-06-30 | E-GEOD-38880 | biostudies-arrayexpress
Project description:Pancreatic cancer is the 3rd most prevalent cause of cancer related deaths in United states alone, with over 55000 patients being diagnosed in 2019 alone and nearly as many succumbing to it. Late detection, lack of effective therapy and poor understanding of pancreatic cancer systemically contributes to its poor survival statistics. Obesity and high caloric intake linked co-morbidities like type 2 diabetes (T2D) have been attributed as being risk factors for a number of cancers including pancreatic cancer. Studies on gut microbiome has shown that lifestyle factors as well as diet has a huge effect on the microbial flora of the gut. Further, modulation of gut microbiome has been seen to contribute to effects of intensive insulin therapy in mice on high fat diet. In another study, abnormal gut microbiota was reported to contribute to development of diabetes in Db/Db mice. Recent studies indicate that microbiome and microbial dysbiosis plays a role in not only the onset of disease but also in its outcome. In colorectal cancer, Fusobacterium has been reported to promote therapy resistance. Certain intra-tumoral bacteria have also been shown to elicit chemo-resistance by metabolizing anti-cancerous agents. In pancreatic cancer, studies on altered gut microbiome have been relatively recent. Microbial dysbiosis has been observed to be associated with pancreatic tumor progression. Modulation of microbiome has been shown to affect response to anti-PD1 therapy in this disease as well. However, most of the studies in pancreatic cancer and microbiome have remained focused om immune modulation. In the current study, we observed that in a T2D mouse model, the microbiome changed significantly as the hyperglycemia developed in these animals. Our results further showed that, tumors implanted in the T2D mice responded poorly to Gemcitabine/Paclitaxel (Gem/Pac) standard of care compared to those in the control group. A metabolomic reconstruction of the WGS of the gut microbiota further revealed that an enrichment of bacterial population involved in drug metabolism in the T2D group.
2020-11-30 | E-MTAB-8739 | biostudies-arrayexpress