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Disruption of transkingdom communication by antibiotics leads to immune and mitochondrial dysfunction in the gut

ABSTRACT: This SuperSeries is composed of the SubSeries listed below. We analyzed the effects of antibiotics using a popular model of gut microbiota depletion in mice by a cocktail of antibiotics. We combined intestinal transcriptome together with metagenomic analysis of the gut microbiota to develop a new bioinformatics approach that probes the links between microbial components and host functions. We found that most antibiotic-induced alterations can be explained by three factors: depletion of the microbiota; direct effects of antibiotics on host tissues; and the effects of remaining antibiotic-resistant microbes. While microbe depletion led to down-regulation of immunity, the two other factors primarily inhibited mitochondrial gene expression and amounts of active mitochondria, and induced cell death. By reconstructing and analyzing a transkingdom network, we discovered that these toxic effects were mediated by virulence/quorum sensing in antibiotic-resistant bacteria.

ORGANISM(S): Mus musculus

PROVIDER: GSE60568 | GEO | 2015/01/26

SECONDARY ACCESSION(S): PRJNA258549

REPOSITORIES: GEO

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Disruption of transkingdom communication by antibiotics leads to immune and mitochondrial dysfunction in the gut

Project description:We analyzed the effects of antibiotics using a popular model of gut microbiota depletion in mice by a cocktail of antibiotics. We combined intestinal transcriptome together with metagenomic analysis of the gut microbiota to develop a new bioinformatics approach that probes the links between microbial components and host functions. We found that most antibiotic-induced alterations can be explained by three factors: depletion of the microbiota; direct effects of antibiotics on host tissues; and the effects of remaining antibiotic-resistant microbes. While microbe depletion led to down-regulation of immunity, the two other factors primarily inhibited mitochondrial gene expression and amounts of active mitochondria, and induced cell death. By reconstructing and analyzing a transkingdom network, we discovered that these toxic effects were mediated by virulence/quorum sensing in antibiotic-resistant bacteria. This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-01-26 | E-GEOD-60568 | biostudies-arrayexpress

Disruption of transkingdom communication by antibiotics leads to immune and mitochondrial dysfunction in the gut (main)

Project description:We analyzed the effects of antibiotics using a popular model of gut microbiota depletion in mice by a cocktail of antibiotics. We combined intestinal transcriptome together with metagenomic analysis of the gut microbiota to develop a new bioinformatics approach that probes the links between microbial components and host functions. We found that most antibiotic-induced alterations can be explained by three factors: depletion of the microbiota; direct effects of antibiotics on host tissues; and the effects of remaining antibiotic-resistant microbes. While microbe depletion led to down-regulation of immunity, the two other factors primarily inhibited mitochondrial gene expression and amounts of active mitochondria, and induced cell death. By reconstructing and analyzing a transkingdom network, we discovered that these toxic effects were mediated by virulence/quorum sensing in antibiotic-resistant bacteria. This series includes gene expression in the ileum of control, antibiotics (ABx)-treated, germfree, germfree-ABx-treated and mice colonized with normal or Abx-resistant microbiota. common reference design with a pool of small intestine RNA labeled with Cy3

2015-01-26 | E-GEOD-60566 | biostudies-arrayexpress

Disruption of transkingdom communication by antibiotics leads to immune and mitochondrial dysfunction in the gut (LMD)

Project description:We analyzed the effects of antibiotics using a popular model of gut microbiota depletion in mice by a cocktail of antibiotics. We combined intestinal transcriptome together with metagenomic analysis of the gut microbiota to develop a new bioinformatics approach that probes the links between microbial components and host functions. We found that most antibiotic-induced alterations can be explained by three factors: depletion of the microbiota; direct effects of antibiotics on host tissues; and the effects of remaining antibiotic-resistant microbes. While microbe depletion led to down-regulation of immunity, the two other factors primarily inhibited mitochondrial gene expression and amounts of active mitochondria, and induced cell death. By reconstructing and analyzing a transkingdom network, we discovered that these toxic effects were mediated by virulence/quorum sensing in antibiotic-resistant bacteria. This series includes gene expression of the laser microdissected compartments of the ileum such as villous epithelium, lamina propria and crypts from specific pathogen free mice common reference design with a pool of small intestine RNA labeled with Cy3

2015-01-26 | E-GEOD-60567 | biostudies-arrayexpress

Disruption of transkingdom communication by antibiotics leads to immune and mitochondrial dysfunction in the gut (main)

Project description:We analyzed the effects of antibiotics using a popular model of gut microbiota depletion in mice by a cocktail of antibiotics. We combined intestinal transcriptome together with metagenomic analysis of the gut microbiota to develop a new bioinformatics approach that probes the links between microbial components and host functions. We found that most antibiotic-induced alterations can be explained by three factors: depletion of the microbiota; direct effects of antibiotics on host tissues; and the effects of remaining antibiotic-resistant microbes. While microbe depletion led to down-regulation of immunity, the two other factors primarily inhibited mitochondrial gene expression and amounts of active mitochondria, and induced cell death. By reconstructing and analyzing a transkingdom network, we discovered that these toxic effects were mediated by virulence/quorum sensing in antibiotic-resistant bacteria. This series includes gene expression in the ileum of control, antibiotics (ABx)-treated, germfree, germfree-ABx-treated and mice colonized with normal or Abx-resistant microbiota.

2015-01-26 | GSE60566 | GEO

Disruption of transkingdom communication by antibiotics leads to immune and mitochondrial dysfunction in the gut (LMD)

Project description:We analyzed the effects of antibiotics using a popular model of gut microbiota depletion in mice by a cocktail of antibiotics. We combined intestinal transcriptome together with metagenomic analysis of the gut microbiota to develop a new bioinformatics approach that probes the links between microbial components and host functions. We found that most antibiotic-induced alterations can be explained by three factors: depletion of the microbiota; direct effects of antibiotics on host tissues; and the effects of remaining antibiotic-resistant microbes. While microbe depletion led to down-regulation of immunity, the two other factors primarily inhibited mitochondrial gene expression and amounts of active mitochondria, and induced cell death. By reconstructing and analyzing a transkingdom network, we discovered that these toxic effects were mediated by virulence/quorum sensing in antibiotic-resistant bacteria. This series includes gene expression of the laser microdissected compartments of the ileum such as villous epithelium, lamina propria and crypts from specific pathogen free mice

2015-01-26 | GSE60567 | GEO

Metabolic and metagenomic outcomes from early-life pulsed antibiotic treatment

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

Metabolic and metagenomic outcomes from early-life pulsed antibiotic treatment

2015-05-07 | GSE68603 | GEO

Intergenerational transfer of antibiotic-perturbed microbiota enhances colitis in susceptible mice.

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

Antibiotics exposure impacts the gut microbiota and influences energy and metabolic homeostasis in Spodoptera frugiperda

Project description:Insect gut microbiota plays important roles in acquiring nutrition, preventing pathogens infection, immune responses, and communicating with the environment. Gut microbiota can be affected by some external factors such as foods, temperature, and antibiotics. Spodoptera frugiperda (Lepidoptera: Noctuidae) is an important destructive pest of grain crops all over the world. The function of gut microbiota in S. frugiperda remains to be investigated. In this study, we fed the S. frugiperda with the antibiotic mixture (penicillin, gentamicin, rifampicin, and streptomycin) to perturb the gut microbiota, and further examined the effect of dysbiosis in gut microbiota on the gene expression of S. frugiperda by RNA sequencing. We found the composition and diversity of the gut bacterial community were changed in S. frugiperda after antibiotics treatmen, and the expression of genes related to energy and metabolic process were affected after antibiotics exposure in S. frugiperda. Our work will help understand the role of gut microbiota in insects.

2021-08-06 | GSE175476 | GEO

Detection of antibiotic resistance genes in human gut microbiota

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

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