Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1268163 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR33801964_1.fastq.gz | Fastqsanger.gz | |||
| SRR33801964_2.fastq.gz | Fastqsanger.gz | |||
| SRR33801965_1.fastq.gz | Fastqsanger.gz | |||
| SRR33801965_2.fastq.gz | Fastqsanger.gz | |||
| SRR33801966_1.fastq.gz | Fastqsanger.gz |
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Project description:Sensing of microbial tryptophan catabolites by the aryl hydrocarbon receptor (AhR) plays a pivotal role in host-microbiome homeostasis by modulating the host immune response. Thereby the involved cellular processes triggered by the metabolites are largely unknown. We analyzed proteomic changes in macrophages trough 24h after treatment with the tryptophan metabolites indole-3-acetic acid (I3AA) or indole-3-aldehyde (IAld), as well as the prototypic AhR-ligand Benzo(a)pyrene (BaP) in the absence and presence of LPS to identify affected processes and pathways.
2021-11-03 | PXD025022 | Pride
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:To study the responses of microbial communities to short-term nitrogen addition and warming,here we examine microbial communities in mangrove sediments subjected to a 4-months experimental simulation of eutrophication with 185 g m-2 year-1 nitrogen addition (N), 3oC warming (W) and nitrogen addition*warming interaction (NW).
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Project description:Morphine causes microbial dysbiosis. In this study we focused on restoration of native microbiota in morphine treated mice and looked at the extent of restoration and immunological consequences of this restoration. Fecal transplant has been successfully used clinically, especially for treating C. difficile infection2528. With our expanding knowledge of the central role of microbiome in maintenance of host immune homeostasis17, fecal transplant is gaining importance as a therapy for indications resulting from microbial dysbiosis. There is a major difference between fecal transplant being used for the treatment of C. difficile infection and the conditions described in our studies. The former strategy is based on the argument that microbial dysbiosis caused by disproportionate overgrowth of a pathobiont can be out-competed by re-introducing the missing flora by way of a normal microbiome transplant. This strategy is independent of host factors and systemic effects on the microbial composition. Here, we show that microbial dysbiosis caused due to morphine can be reversed by transplantation of microbiota from the placebo-treated animals.
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Project description:Bacterial and archaeal communities in mangrove sediments under oil contamination and nitrate stimulation
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Project description:Morphine and its pharmacological derivatives are the most prescribed analgesics for moderate to severe pain management. However, chronic use of morphine reduces pathogen clearance and induces bacterial translocation across the gut barrier. The enteric microbiome has been shown to play a critical role in the preservation of the mucosal barrier function and metabolic homeostasis. Here, we show for the first time, using bacterial 16s rDNA sequencing, that chronic morphine treatment significantly alters the gut microbial composition and induces preferential expansion of the gram-positive pathogenic and reduction of bile-deconjugating bacterial strains. A significant reduction in both primary and secondary bile acid levels was seen in the gut, but not in the liver with morphine treatment. Morphine induced microbial dysbiosis and gut barrier disruption was rescued by transplanting placebo-treated microbiota into morphine-treated animals, indicating that microbiome modulation could be exploited as a therapeutic strategy for patients using morphine for pain management. In this study, we establish a link between the two phenomena, namely gut barrier compromise and dysregulated bile acid metabolism. We show for the first time that morphine fosters significant gut microbial dysbiosis and disrupts cholesterol/bile acid metabolism. Changes in the gut microbial composition is strongly correlated to disruption in host inflammatory homeostasis13,14 and in many diseases (e.g. cancer/HIV infection), persistent inflammation is known to aid and promote the progression of the primary morbidity. We show here that chronic morphine, gut microbial dysbiosis, disruption of cholesterol/bile acid metabolism and gut inflammation; have a linear correlation. This opens up the prospect of devising minimally invasive adjunct treatment strategies involving microbiome and bile acid modulation and thus bringing down morphine-mediated inflammation in the host.
2016-06-01 | E-MTAB-3722 | biostudies-arrayexpress
Project description:Background: Toll-like receptor 2 (TLR2) plays a pivotal role in innate immunity and has recently emerged as a criti-cal regulator of host-microbiome interactions. However, how TLR2 influences host transcriptional responses to colonized microbiome and microbial community dynamics remains largely unclear. Germ free (GF) and conven-tionalized zebrafish (Danio rerio) model provides a valuable system to study microbiome functions. Results: RNAseq analysis revealed that transcriptomic alterations resulted from tlr2 mutation were more extensive in the presence of the microbiome than under the GF condition, indicating that tlr2 mutation has a more pro-nounced impact on host transcriptional responses when microbial signals are present. KEGG enrichment analyses showed an enhanced host response to the energy metabolism in the presence of microbial stimuli resulting from tlr2 deficiency. In addition, microbiome colonization elicited a broader transcriptional response in tlr2 wild-type larvae than in the mutants, highlighting the essential role of tlr2 in regulating host transcriptomic programs in re-sponse to microbial signals. In terms of how tlr2 influences microbial composition, 16S rRNA gene sequencing showed that tlr2 mutants exhibited higher microbial diversity during early development, whereas adult microbial diversity was highest in wild-type males, indicating a developmental stage- and sex-specific restructuring of the gut microbiome. For larvae at the genus level, tlr2 mutant larvae showed increased Chryseobacterium and Flecto-bacillus but reduced Gracilibacteria abundance relative to wild-type controls. For adult gut samples, the relative abundance of Cetobacterium was lower, while genera such as Romboutsia, Aeromonas and Pseudarthrobacter were more abundant in tlr2 wild-type male group compared to other groups. Predicted functional analyses revealed that tlr2 deficiency induced complex alterations in microbial metabolic pathways, with distinct pathway enrichments observed between larval and adult stages. Conclusions: TLR2 not only modulates host transcriptional responses to microbial colonization but also shapes gut microbial diversity, composition, and metabolic potential. Our findings highlight the critical role of TLR2 in orchestrating immunometabolic homeostasis and provide new insights into its broader function in maintaining host-microbiota symbiosis across developmental stages.
2025-07-31 | GSE303417 | GEO
Project description:The environmental accumulation of polycyclic aromatic hydrocarbons (PAHs), such as benzo(a)pyrene (BaP), poses significant threats to ecosystems and public health due to their persistent nature, mutagenic potential, and well-documented carcinogenicity. In this study, we investigated the ability of the extremophilic yeast Debaryomyces hansenii to activate specialized detoxification mechanisms for BaP degradation, even under nutrient-deprived conditions. When exposed to 100 ppm BaP, D. hansenii eliminated over 70% of the contaminant within three days while maintaining normal growth dynamics. RNA-Seq analysis revealed widespread transcriptional remodeling, with 1179 genes upregulated and 1031 downregulated under BaP-only conditions, and 1067 upregulated and 977 downregulated genes during co-metabolic exposure (2% glucose + 100 ppm BaP), from a total of 6506 annotated genes. Gene Ontology (GO) and KEGG enrichment analyses highlighted the activation of xenobiotic degradation pathways, notably involving cytochrome P450 monooxygenases (CYPs), epoxide hydrolases (EHs), and glutathione S-transferases (GSTs), alongside an enhanced antioxidant response and finely tuned glutathione homeostasis. This work provides the first comprehensive transcriptomic profile of BaP detoxification in D. hansenii, revealing an intricate and highly adaptive stress response. Collectively, these findings position D. hansenii as a promising eukaryotic platform for bioremediation in saline and contaminated environments, especially where conventional microbial candidates fall short due to environmental extremes or nutrient scarcity.
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Project description:Here we report a direct tRNA sequencing protocol and software to simultaneously examine the composition and biological activity of naturally occurring microbial communities. Our analysis of mouse gut microbiome with tRNA-seq and 16S ribosomal RNA gene amplicons revealed comparable microbial community structures, and additional physiological insights into the microbiome through tRNA abundance and modifications.
2018-11-09 | GSE100263 | GEO
Project description:The intestinal microbiome has been associated with response to immune checkpoint inhibitors (ICI) in humans, and causally implicated in ICI responsiveness in animal models. Therapeutic augmentation of the microbiome in ICI recipients is being investigated in multiple ongoing human clinical trials. We conducted an early phase clinical trial of a cultivated, orally-delivered 30-species microbial consortium (microbial ecosystem therapeutic-4, MET4) designed for co-administration with ICIs and assessed safety, tolerability and ecological responses in patients with advanced solid tumors.
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