Ontology highlight
ABSTRACT:
PROVIDER: PRJNA753800 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15414889_1.fastq.gz | Fastqsanger.gz | |||
| SRR15414889_2.fastq.gz | Fastqsanger.gz | |||
| SRR15414890_1.fastq.gz | Fastqsanger.gz | |||
| SRR15414890_2.fastq.gz | Fastqsanger.gz | |||
| SRR15414891_1.fastq.gz | Fastqsanger.gz |
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Project description:We used a DNA microarray chip covering 369 resistance types to investigate the relation of antibiotic resistance gene diversity with humans’ age. Metagenomic DNA from fecal samples of 123 healthy volunteers of four different age groups, i.e. pre-school Children (CH), School Children (SC), High School Students (HSS) and Adults (AD) were used for hybridization. The results showed that 80 different gene types were recovered from the 123 individuals gut microbiota, among which 25 were present in CH, 37 in SC, 58 in HSS and 72 in AD. Further analysis indicated that antibiotic resistance genes in groups of CH, SC and AD can be independently clustered, and those ones in group HSS are more divergent. The detailed analysis of antibiotic resistance genes in human gut is further described in the paper DNA microarray analysis reveals the antibiotic resistance gene diversity in human gut microbiota is age-related submitted to Sentific Reports
2014-01-16 | GSE54070 | GEO
Project description:We used a DNA microarray chip covering 369 resistance types to investigate the relation of antibiotic resistance gene diversity with humansM-bM-^@M-^Y age. Metagenomic DNA from fecal samples of 123 healthy volunteers of four different age groups, i.e. pre-school Children (CH), School Children (SC), High School Students (HSS) and Adults (AD) were used for hybridization. The results showed that 80 different gene types were recovered from the 123 individuals gut microbiota, among which 25 were present in CH, 37 in SC, 58 in HSS and 72 in AD. Further analysis indicated that antibiotic resistance genes in groups of CH, SC and AD can be independently clustered, and those ones in group HSS are more divergent. The detailed analysis of antibiotic resistance genes in human gut is further described in the paper DNA microarray analysis reveals the antibiotic resistance gene diversity in human gut microbiota is age-related submitted to Sentific Reports The antibiotic resistance gene microarray is custom-designed (Roche NimbleGen), based on a single chip containing 3 internal replicated probe sets of 12 probes per resistance gene, covering the whole 315K 12-plex platform spots.
2014-01-16 | E-GEOD-54070 | biostudies-arrayexpress
Project description:We wanted to identify effector molecules which confer rotavirus resistance in microbiota-depleted mice We used microarrays to analyze the global programme of gene expression in response to IL22 treatment in the ileum of antibiotic-treated Ifnlr1-/- mice
2021-08-03 | GSE166400 | GEO
Project description:Mammalian species have co-evolved with intestinal microbial communities that can shape development and adapt to environmental changes, including antibiotic perturbation or nutrient flux. In humans, especially children, microbiota disruption is common, yet the dynamic microbiome recovery from early-life antibiotics is still uncharacterized. Using a mouse model mimicking pediatric antibiotic use, we found that therapeutic-dose pulsed antibiotic treatment (PAT) with a beta-lactam or macrolide altered both host and microbiota development. Early-life PAT accelerated total mass and bone growth, and resulted in progressive changes in gut microbiome diversity, population structure, and metagenomic content, with microbiome effects dependent on the number of courses and class of antibiotic. While control microbiota rapidly adapted to a change in diet, PAT slowed the ecological progression, with delays lasting several months in response to the macrolide. This study identifies key markers of disturbance and recovery, which may help provide therapeutic targets for microbiota restoration following antibiotic treatment. C57BL/6J mice received three antibiotic courses: at days 10-15, 28-31, and 37-40 of life, amoxicillin or tylosin.Livers were collected at age 22 weeks, RNA was extracted, and transcriptional differences were measured by microarray analysis.
2015-05-07 | E-GEOD-68603 | biostudies-arrayexpress
Project description:<p>The study of antimicrobial resistance (AMR) in infectious diarrhea has generally been limited to cultivation, antimicrobial susceptibility testing and targeted PCR assays. When individual strains of significance are identified, whole genome shotgun (WGS) sequencing of important clones and clades is performed. Genes that encode resistance to antibiotics have been detected in environmental, insect, human and animal metagenomes and are known as "resistomes". While metagenomic datasets have been mined to characterize the healthy human gut resistome in the Human Microbiome Project and MetaHIT and in a Yanomani Amerindian cohort, directed metagenomic sequencing has not been used to examine the epidemiology of AMR. Especially in developing countries where sanitation is poor, diarrhea and enteric pathogens likely serve to disseminate antibiotic resistance elements of clinical significance. Unregulated use of antibiotics further exacerbates the problem by selection for acquisition of resistance. This is exemplified by recent reports of multiple antibiotic resistance in Shigella strains in India, in Escherichia coli in India and Pakistan, and in nontyphoidal Salmonella (NTS) in South-East Asia. We propose to use deep metagenomic sequencing and genome level assembly to study the epidemiology of AMR in stools of children suffering from diarrhea. Here the epidemiology component will be surveillance and analysis of the microbial composition (to the bacterial species/strain level where possible) and its constituent antimicrobial resistance genetic elements (such as plasmids, integrons, transposons and other mobile genetic elements, or MGEs) in samples from a cohort where diarrhea is prevalent and antibiotic exposure is endemic. The goal will be to assess whether consortia of specific mobile antimicrobial resistance elements associate with species/strains and whether their presence is enhanced or amplified in diarrheal microbiomes and in the presence of antibiotic exposure. This work could potentially identify clonal complexes of organisms and MGEs with enhanced resistance and the potential to transfer this resistance to other enteric pathogens.</p> <p>We have performed WGS, metagenomic assembly and gene/protein mapping to examine and characterize the types of AMR genes and transfer elements (transposons, integrons, bacteriophage, plasmids) and their distribution in bacterial species and strains assembled from DNA isolated from diarrheal and non-diarrheal stools. The samples were acquired from a cohort of pediatric patients and controls from Colombia, South America where antibiotic use is prevalent. As a control, the distribution and abundance of AMR genes can be compared to published studies where resistome gene lists from healthy cohort sequences were compiled. Our approach is more epidemiologic in nature, as we plan to identify and catalogue antimicrobial elements on MGEs capable of spread through a local population and further we will, where possible, link mobile antimicrobial resistance elements with specific strains within the population.</p>
| phs001260 | dbGaP
Project description:Antibiotics are thought to affect host physiology by altering the gut microbiota. But which effects of antibiotics are microbiota-dependent or -independent is not clear. Here, we present a resource encompassing host and microbiota response to antibiotic treatment and computational tools to analyze them. We show how antibiotic administration routes affect host and microbiota responses and how combining antibiotics alters their individual activity. We developed CompoRes, a tool to determine whether perturbation affects the host directly or via the microbiota, and discovered microbiota-independent effects of antibiotic treatment. We found that circadian expression of MHC class II in the colon is functional in germ-free mice and is controlled by feeding via glucose. This expression pattern was lost during vancomycin treatment as the antibiotic altered feeding behaviour in a microbiota-independent manner. Together, our study provides tools for analysis of host response to different microbiota compositions which can also identify microbiota-independent effects of perturbations.
2026-07-02 | GSE293363 | GEO
Project description:Antibiotics are thought to affect host physiology by altering the gut microbiota. But which effects of antibiotics are microbiota-dependent or -independent is not clear. Here, we present a resource encompassing host and microbiota response to antibiotic treatment and computational tools to analyze them. We show how antibiotic administration routes affect host and microbiota responses and how combining antibiotics alters their individual activity. We developed CompoRes, a tool to determine whether perturbation affects the host directly or via the microbiota, and discovered microbiota-independent effects of antibiotic treatment. We found that circadian expression of MHC class II in the colon is functional in germ-free mice and is controlled by feeding via glucose. This expression pattern was lost during vancomycin treatment as the antibiotic altered feeding behaviour in a microbiota-independent manner. Together, our study provides tools for analysis of host response to different microbiota compositions which can also identify microbiota-independent effects of perturbations.
2026-07-02 | GSE293180 | GEO
Project description:Antibiotics are thought to affect host physiology by altering the gut microbiota. But which effects of antibiotics are microbiota-dependent or -independent is not clear. Here, we present a resource encompassing host and microbiota response to antibiotic treatment and computational tools to analyze them. We show how antibiotic administration routes affect host and microbiota responses and how combining antibiotics alters their individual activity. We developed CompoRes, a tool to determine whether perturbation affects the host directly or via the microbiota, and discovered microbiota-independent effects of antibiotic treatment. We found that circadian expression of MHC class II in the colon is functional in germ-free mice and is controlled by feeding via glucose. This expression pattern was lost during vancomycin treatment as the antibiotic altered feeding behaviour in a microbiota-independent manner. Together, our study provides tools for analysis of host response to different microbiota compositions which can also identify microbiota-independent effects of perturbations.
2026-07-02 | GSE293029 | GEO
Project description:Antibiotics are thought to affect host physiology by altering the gut microbiota. But which effects of antibiotics are microbiota-dependent or -independent is not clear. Here, we present a resource encompassing host and microbiota response to antibiotic treatment and computational tools to analyze them. We show how antibiotic administration routes affect host and microbiota responses and how combining antibiotics alters their individual activity. We developed CompoRes, a tool to determine whether perturbation affects the host directly or via the microbiota, and discovered microbiota-independent effects of antibiotic treatment. We found that circadian expression of MHC class II in the colon is functional in germ-free mice and is controlled by feeding via glucose. This expression pattern was lost during vancomycin treatment as the antibiotic altered feeding behaviour in a microbiota-independent manner. Together, our study provides tools for analysis of host response to different microbiota compositions which can also identify microbiota-independent effects of perturbations.
2026-07-02 | GSE324684 | GEO
Project description:Antibiotics have long-lasting consequences on the gut microbiota with the potential to impact host physiology and health. However, little is known about the transgenerational impact of an antibiotic-perturbed microbiota. Here we demonstrated that adult pregnant female mice inoculated with a gut microbial community shaped by antibiotic exposure passed on their dysbiotic microbiota to their offspring. This dysbiotic microbiota remained distinct from controls for at least 5 months in the offspring without any continued exposure to antibiotics. By using IL-10 deficient mice, which are genetically susceptible to colitis, we showed mice that received an antibiotic-perturbed gut microbiota from their mothers had increased risk of colitis. Taken together, our findings indicate that the consequences of antibiotic exposure affecting the gut microbiota can extend to a second generation.
2017-12-01 | GSE92623 | GEO