Oral Administration of XXXX Induces Dysbiosis of Gut Microbiota and Impaired Barrier Function Leading to Dissemination of Enterobacteria to the Liver.

@entity32 @entity5694 @entity19 @entity262 @entity2521 @entity40672 @entity2523
UNASSIGNED: Although @entity2521 has been implicated as a risk factor for various @entity262 , the precise mechanisms by which @entity2521 induces @entity262 remain to be elucidated. We have previously revealed that repeated oral administration of @entity2523 elicits @entity5694 via changes in the gut microbiota of the ileum, and thereby induces systemic @entity32 and insulin resistance. However, it is not clear to what extent a single administration of @entity2523 could affect gut microbiota composition, gut barrier function, and subsequent influx of gut microbiota into the liver. Therefore, in the present study, C57BL/6 @entity19 were orally administered @entity40672 ) once and compared to sham-inoculated @entity19 . The phylogenetic structure and diversity of microbial communities in the gut and liver were analyzed by pyrosequencing the 16S ribosomal RNA genes. Serum endotoxin activity was determined by a Limulus amebocyte lysate test. Gene expression in the intestine and expression of 16S rRNA genes in the blood and liver were examined by quantitative polymerase chain reaction. Administration of @entity2523 significantly altered gut microbiota, with an increased proportion of phylum Bacteroidetes, a decreased proportion of phylum Firmicutes, and increased serum endotoxin levels. In the intestinal tissues, gene expression of tjp-1 and occludin, which are involved in intestinal permeability, were downregulated. Higher amounts of bacterial DNA were detected in the liver of infected @entity19 . Importantly, changes in gut microbiota preceded systemic inflammatory changes. These results further support the idea that disturbance of the gut microbiota composition by orally derived periodontopathic bacteria may be a causal mechanism linking @entity2521 and @entity262 .
