Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1150211 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30315329.fastq.gz | Fastqsanger.gz | |||
| SRR30315330.fastq.gz | Fastqsanger.gz | |||
| SRR30315331.fastq.gz | Fastqsanger.gz | |||
| SRR30315332.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 4 of 4 |
Similar Datasets
Project description:Human Gut Microbiota Dynamics in Response to Panchkarma Therapy
| PRJNA1147244 | ENA
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
Project description:Gut microbiota has been associated with carcinogenesis and immune regulation. While there is evidence supporting its influence on immunotherapy response in melanoma, its impact on BRAF/MEK-targeted therapy remains unexplored. This study assessed gut microbiota composition and immune-associated genes in melanoma, to generate hypothesis on prognostic and predictive biomarkers for BRAF/MEK inhibitor therapy. We hypothesize that GM composition may influence responses to treatment or toxicity in patients receiving iBRAF/MEK therapy. Specific microorganisms may serve as prognostic or predictive biomarkers of response, as well as of treatment-related adverse events. Additionally, genes associated with immune activation could further refine prognostic and predictive models. By identifying biomarkers for early prediction of response and microorganisms linked to treatment efficacy and toxicity, our findings aim to contribute to the development of microbiota-modulation strategies that could enhance therapeutic outcomes in specific contexts.
2025-06-06 | GSE299194 | GEO
Project description:Adequate sleep is essential for relieving stress and rejuvenating the mind; however, undesirable physiological and pathological responses resulting from sleep insufficiency or sleep deprivation (SD) are becoming increasingly common. However, the influence of sleep deficiency on gut microbiota and microbiota-associated human diseases, especially on cardiac diseases remain controversial. Here, we constructed the experimental SD model in mice and found it significantly resulted in weakness, depression-like behaviors, and multiple organs dysfunction. Intriguingly, SD mice developed pathogenic cardiac hypertrophy and fibrosis with poor ejection fraction as well as fractional shortening. 16s rRNA sequencing demonstrated that SD-induced the pathogenic effects of gut microbiota, which was also observed in mice received by fecal microbe from SD mice in fecal microbiota transplantation (FMT) assays. Next, we investigated the therapeutic effects and underlying mechanisms of oxygen therapy in gut microbiota-associated cardiac fibrosis and dysfunction. The environment of 30% oxygen concentration effectively ameliorated the pathological effects on cardiac function. Transcriptome data also found oxygen therapy targeted several hypoxia-dependent pathways and suppressed cardiac collagen production. In conclusion, these results indicated the importance of sufficient sleep in gut microbiota and may represent a potential therapeutic strategy of oxygen environment exerts protective effects in sleepless sufferings through gut microbiota.
2025-03-25 | GSE284746 | GEO
Project description:The gut microbiota influences both local and systemic inflammation. Inflammation contributes to development, progression and treatment of cancer, but it remains unclear whether commensal bacteria affect inflammation in the sterile tumor microenvironment. Here we show that disruption of the microbiota impairs the response of subcutaneous tumors to CpG-oligonucleotide immunotherapy and platinum chemotherapy. In antibiotic-treated or germ-free mice, tumor-infiltrating myeloid-derived cells responded poorly to therapy, resulting in lower cytokine production and tumor necrosis after CpG-oligonucleotide treatment, and deficient production of reactive oxygen species and cytotoxicity following chemotherapy. Thus, optimal responses to cancer therapy require an intact commensal microbiota that mediates its effects by modulating myeloid-derived cell functions in the tumor microenvironment. These findings underscore the importance of the microbiota in the outcome of disease treatment. Oxaliplatin treatment induces expression of pro-inflammatory genes, which are inhibited by antibiotic pretreatment. Our goal was to ascertain the effect of antibiotic on the tumor gene expression profile prior to treatment and early on after the treatment with chemotherapy (oxaliplatin). The time points were selected t
2013-12-03 | E-GEOD-51414 | biostudies-arrayexpress
Project description:Changes in microbiome composition have been associated with a wide array of human diseases, turning the human microbiota into an attractive target for therapeutic intervention. Yet clinical translation of these findings requires the establishment of causative connections between specific microbial taxa and their functional impact on host tissues. Here, we infused gut organ cultures with longitudinal microbiota samples collected from therapy-naïve irritable bowel syndrome (IBS) patients under low-FODMAP (fermentable Oligo-, Di-, Mono-saccharides and Polyols) diet. We show that post-diet microbiota regulates intestinal expression of inflammatory and neuro-muscular gene-sets. Specifically, we identify Bifidobacterium adolescentis as a diet-sensitive pathobiont that alters tight junction integrity and disrupts gut barrier functions. Collectively, we present a unique pathway discovery approach for mechanistic dissection and identification of functional diet-host-microbiota modules. Our data support the hypothesis that the gut microbiota mediates the beneficial effects of low-FODMAP diet and reinforce the potential feasibility of microbiome based-therapies in IBS.
2022-10-14 | GSE215048 | GEO
Project description:Changes in microbiome composition have been associated with a wide array of human diseases, turning the human microbiota into an attractive target for therapeutic intervention. Yet clinical translation of these findings requires the establishment of causative connections between specific microbial taxa and their functional impact on host tissues. Here, we infused gut organ cultures with longitudinal microbiota samples collected from therapy-naïve irritable bowel syndrome (IBS) patients under low-FODMAP (fermentable Oligo-, Di-, Mono-saccharides and Polyols) diet. We show that post-diet microbiota regulates intestinal expression of inflammatory and neuro-muscular gene-sets. Specifically, we identify Bifidobacterium adolescentis as a diet-sensitive pathobiont that alters tight junction integrity and disrupts gut barrier functions. Collectively, we present a unique pathway discovery approach for mechanistic dissection and identification of functional diet-host-microbiota modules. Our data support the hypothesis that the gut microbiota mediates the beneficial effects of low-FODMAP diet and reinforce the potential feasibility of microbiome based-therapies in IBS.
2022-10-14 | GSE215047 | GEO
Project description:Changes in microbiome composition have been associated with a wide array of human diseases, turning the human microbiota into an attractive target for therapeutic intervention. Yet clinical translation of these findings requires the establishment of causative connections between specific microbial taxa and their functional impact on host tissues. Here, we infused gut organ cultures with longitudinal microbiota samples collected from therapy-naïve irritable bowel syndrome (IBS) patients under low-FODMAP (fermentable Oligo-, Di-, Mono-saccharides and Polyols) diet. We show that post-diet microbiota regulates intestinal expression of inflammatory and neuro-muscular gene-sets. Specifically, we identify Bifidobacterium adolescentis as a diet-sensitive pathobiont that alters tight junction integrity and disrupts gut barrier functions. Collectively, we present a unique pathway discovery approach for mechanistic dissection and identification of functional diet-host-microbiota modules. Our data support the hypothesis that the gut microbiota mediates the beneficial effects of low-FODMAP diet and reinforce the potential feasibility of microbiome based-therapies in IBS.
2022-10-14 | GSE215049 | GEO
Project description:The human gut microbiota is crucial for degrading dietary fibres from the diet. However, some of these bacteria can also degrade host glycans, such as mucins, the main component of the protective gut mucus layer. Specific microbiota species and mucin degradation patterns are associated with inflammatory processes in the colon. Yet, it remains unclear how the utilization of mucin glycans affects the degradation of dietary fibres by the human microbiota. Here, we used three dietary fibres (apple pectin, β-glucan and xylan) to study in vitro the dynamics of colon mucin and dietary fibre degradation by the human faecal microbiota. The dietary fibres showed clearly distinguishing modulatory effects on faecal microbiota composition. The utilization of colon mucin in cultures led to alterations in microbiota composition and metabolites. Metaproteome analysis showed the central role of the Bacteroides in degradation of complex fibres while Akkermansia muciniphila was the main degrader of colonic mucin. This work demonstrates the intricacy of complex glycan metabolism by the gut microbiota and how the utilization of host glycans leads to alterations in the metabolism of dietary fibres. Metaproteomics analysis of this data reveals the functional activities of the bacteria in consortia, by this contributing to a better understanding of the complex metabolic pathways within the human microbiota that can be manipulated to maximise beneficial microbiota-host interactions.
2024-06-13 | PXD035981 | Pride
Project description:The postnatal period is one of the important windows for developing the gastrointestinal tract's structure-function and associated mucosal immunity. Recent studies suggest a promising contribution of gut microbiota in maintaining host health, immunity, and gut development. However, the function of postnatal gut microbiota dynamics concerning intestinal mucosal development needs to be better understood. To decipher the causal role of gut microbiota on barrier integrity and intestinal epithelium development, we executed an antibiotic-mediated perturbation and tracked the kinetics in postnatal mice. We observed a postnatal age-related impact of antibiotic-mediated gut microbiota perturbation with a substantial decrease in total bacterial load on P14D and also in the barrier integrity and IECs marker. To enhance our knowledge of the mechanisms behind this, we employed a global transcriptomics approach to see the alterations in the mucosal innate immunity and other relevant pathways.
2025-02-08 | GSE255472 | GEO