title: Comparing the effects of acute alcohol consumption in germ-free and conventional mice: the role of the gut microbiota.
abstract: BACKGROUND
  Increasing evidence suggest that the gut microbiota plays an important role in liver pathology after acute alcohol intake. The aim of our study was to investigate the roles played by commensal bacteria in alcohol-induced liver injury and in the dysbiosis caused by alcohol intake in germ-free mice, as well as the possibility of protection against alcohol-induced injuries in animals fed a high-fiber diet. For these purposes, germ-free and conventional mice were submitted to acute alcohol intake, consisting of administration of ethanol in their drinking water for 7 days, with a higher dose of alcohol administered on day 7.
  
  
  RESULTS
  There was no liver injury after alcohol consumption, and there was less neutrophil infiltration and lower pro-inflammatory cytokine levels (CXCL-1/KC and interleukin (IL)-6) in the liver in germ-free mice compared with alcohol-fed conventional mice. Additionally, conventionalization of germ-free mice with intestinal contents from alcohol-fed conventional mice induced injury and inflammation in both the liver and the intestine, suggesting that alcohol intake successively caused a perturbation of the intestinal microbiota (dysbiosis) and liver injury. Finally, previous treatment with a high-fiber diet decreased liver injury and gut permeability in alcohol-fed conventional mice.
  
  
  CONCLUSIONS
  In conclusion, the results of the present study provide evidence that the gut microbiota plays an important role in alcohol-induced liver injury, apparently through dysbiosis of the intestinal microbial ecosystem caused by alcohol intake. Furthermore, treatment with a high-fiber diet can counteract hepatocyte pathology and gut leakage and thus could be a promising therapeutic option.
authors.forename: Canesso
authors.initials: C
authors.lastname: M C C
authors.forename: Lacerda
authors.initials: L
authors.lastname: N L
authors.forename: Ferreira
authors.initials: F
authors.lastname: C M
authors.forename: Gonçalves
authors.initials: G
authors.lastname: J L
authors.forename: Almeida
authors.initials: A
authors.lastname: D
authors.forename: Gamba
authors.initials: G
authors.lastname: C
authors.forename: Cassali
authors.initials: C
authors.lastname: G
authors.forename: Pedroso
authors.initials: P
authors.lastname: S H
authors.forename: Moreira
authors.initials: M
authors.lastname: C
authors.forename: Martins
authors.initials: M
authors.lastname: F S
authors.forename: Nicoli
authors.initials: N
authors.lastname: J R
authors.forename: Teixeira
authors.initials: T
authors.lastname: M M
authors.forename: Godard
authors.initials: G
authors.lastname: A L B
authors.forename: Vieira
authors.initials: V
authors.lastname: A T
mesh_terms: D000428:Alcohol Drinking / Q000009:adverse effects*; D000818:Animals; D054360:Chemokine CXCL1 / Q000378:metabolism; D059305:Diet, High-Fat; D000431:Ethanol / Q000009:adverse effects*; D005260:Female; D005856:Germ-Free Life / Q000502:physiology; D007249:Inflammation / Q000139:chemically induced / Q000378:metabolism / Q000382:microbiology; D015850:Interleukin-6 / Q000378:metabolism; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000382:microbiology*; D008099:Liver / Q000378:metabolism / Q000382:microbiology / Q000473:pathology*; D008107:Liver Diseases / Q000378:metabolism / Q000382:microbiology / Q000473:pathology*; D051379:Mice; D064307:Microbiota / Q000502:physiology*; D010539:Permeability
chemical_list: D054360:Chemokine CXCL1; D015850:Interleukin-6; D000431:Ethanol