Ontology highlight
ABSTRACT:
PROVIDER: PRJNA913918 | ENA |
REPOSITORIES: ENA
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Project description:The gut microbiota impacts many aspects of host biology including immune function. One hypothesis is that microbial communities induce epigenetic changes with accompanying alterations in chromatin accessibility, providing a mechanism that allows a community to have sustained host effects even in the face of its structural or functional variation. We used ATAC-seq to define chromatin accessibility in predicted enhancer regions of intestinal αβ+ and γδ+ intraepithelial lymphocytes (IELs) purified from germ-free mice, their conventionally-raised (CONV-R) counterparts, and mice reared GF and then colonized with a CONV-R gut microbiota at the end of the suckling-weaning transition. Characterizing genes adjacent to traditional enhancers and super-enhancers revealed signaling networks, metabolic pathways, and enhancer-associated transcription factors affected by the microbiota. Our results support the notion that epigenetic modifications help define microbial community-affiliated functional features of host immune cell lineages.
2016-11-28 | GSE89646 | GEO
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:The gut-brain axis allows gut microbes to influence host social behavior, yet the specific role of microbial genetic variation in this process and its potential transgenerational effects remains poorly understood. Using C. elegans as a model, we identified 77 E. coli strains among 3,983 mutants that markedly enhanced C. elegans aggregation behavior. Our findings reveal that mutant bacteria modulate C. elegans social behavior through distinct neurobehavioral pathways, demonstrating a synergistic regulatory mechanism between microbial genetics and host heredity. Mechanistically, ycgJ mutant bacteria were found to impact C. elegans social behavior via the mitochondrial pathway. Additionally, even F2 offspring of parent C. elegans exposed to these mutant bacteria exhibited enhanced social behavior within their populations. These insights underscore the significance of investigating microbial genetic variation in relation to host behavior, particularly for the development of genetically engineered probiotics, aimed at promoting well-being across generations.
2025-01-27 | GSE283454 | GEO
Project description:Single nucleotide polymorphisms (SNPs) are the most common type of genetic variation in gut microbial metagenome and host genome but they could not adequately represent the protein-level variants. Single amino-acid polymorphisms (SAP) derived from non-synonymous SNPs can cause functional changes of proteins and are important forces of adaption. However, SAP remain quite unexplored for human gut microbiome. Here, we present a comprehensive large-scale analysis of SAP in the gut ecosystem, introducing a rigorous computational pipeline for detecting such protein variation from 992 published human metaproteomes.
2025-04-05 | PXD062661 |
Project description:Diet-induced obesity (DIO) is rapidly becoming a global health problem, particularly as Westernization of emerging nations continues. Currently, one third of adult Americans are considered obese and, if current trends continue, >90% of US citizens are predicted to be affected by 2050. However, efforts to fight this epidemic have not yet produced sound solutions for prevention or treatment. Our studies reveal a balanced and chronobiological relationship between food consumption, daily variation in gut microbial evenness and function, basomedial hypothalamic circadian clock (CC) gene expression, and key hepatic metabolic regulatory networks , including CC and nuclear receptors (NR), that is are essential for metabolic homeostasis. “Western” diets high in saturated fats dramatically alter diurnal variation in microbial composition and function, which in turn lead to uncoupling of the hepatic CC and NR networks from central CC control in ways that offset the timing and types of regulatory factors directing metabolic function. These signals include microbial metabolites such as short chain fatty acids (SCFAs) and hydrogen sulfide (H2S) that can directly regulate or disrupt metabolic networks of the hepatocyte. Our study therefore provides insights into the complex and dynamic relationships between diet, gut microbes, and the host that are critical for maintenance of health. Perturbations of this constellation of processes, in this case by diet-induced dysbiosis and its metabolomic signaling, can potentially promote metabolic imbalances and disease. This knowledge opens up many possibilities for novel therapeutic and interventional strategies to treat and prevent DIO, ranging from the manipulation of gut microbial function to pharmacological targeting of host pathways to restore metabolic balance. Mice were raised under germ-free or specific pathogen-free condition, or germ-free followed by conventionization. Liver tissues were harvested for total RNA isolation and hybridization on Affymetrix microarrays
2013-12-24 | E-GEOD-53590 | biostudies-arrayexpress
Project description:Subjects with different allergic phenotypes showed distinct gut microbial patterns and functions. AD+FA subjects showed the mixtures of gut microbial patterns of FA and AD, while gut microbial pattern of FA seems to dominate in subjects with AD+FA
| PXD027692 | JPOST Repository
Project description:Epigenetic mechanisms are increasingly recognized as critical regulators of host-microbiota interactions. Here, we report that intestinal epithelial-specific deletion of Tet2, a key DNA demethylase, leads to structural abnormalities, impaired barrier function, and remarkable reprogramming of the gut microbial community. Mechanistically, Tet2 deficiency significantly downregulated the expression of the apical sodium-dependent bile acid transporter (ASBT/Slc10a2), resulting in altered bile acid homeostasis with specific accumulation of hyocholic acid (HCA) in the intestinal lumen. This metabolic shift created a favorable niche for selective expansion of bile salt hydrolase (BSH)-expressing Lactobacillus species. Furthermore, we identified an age-dependent regulatory role of HCA in shaping microbial composition, promoting Lactobacillus in young mice while enriching Akkermansia in aged animals. Our findings unveil an epigenetic-metabolic-microbial axis centered on Tet2-mediated regulation of bile acid metabolism, providing new insights into how host epigenetic factors shape the gut microbial ecosystem.
2026-01-13 | GSE307332 | GEO
Project description:Dietary phytochemicals are plant-derived bioactive compounds that can influence host physiology and gut microbial communities. However, the structural distinctiveness of phytochemicals and their modulation of host intestinal gene expression in a sex-dependent manner remain poorly understood. In this study, we used Drosophila melanogaster to investigate gut transcriptomic responses to four phytochemical-enriched diets, capsaicin, curcumin, resveratrol, and thymoquinone. Two-day-old mated female and male flies were exposed to control or phytochemical-supplemented diets for 10 days, after which gut tissues were dissected for bulk RNA sequencing. Transcriptomic analysis revealed that biological sex was a major source of variation in the gut, with female and male flies showing distinct expression profiles across dietary treatments. Phytochemical supplementation induced compound and sex-specific transcriptional responses. Curcumin produced the strongest transcriptional response, with females showing reduced expression of genes involved in carbohydrate digestion and trehalose metabolism, whereas males showed enrichment of xenobiotic detoxification pathways dominated by cytochrome P450 genes. Capsaicin also induced sex-dependent responses, including detoxification-associated transcriptional changes in females and increased expression of immune-related genes in males. These results indicate that dietary phytochemicals elicit sex-specific gut transcriptomic responses in Drosophila melanogaster and highlight biological sex as an important variable in studies of diet-host interactions.
2026-05-11 | GSE330166 | GEO