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

ABSTRACT: 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

ORGANISM(S): Mus musculus

SUBMITTER: Natalia Shulzhenko 

PROVIDER: E-GEOD-60567 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress