title: Effects of Salmonella infection on hepatic damage following acute liver injury in rats.
abstract: BACKGROUND
  Acute liver injury is a common clinical disorder associated with intestinal barrier injury and disturbance of intestinal microbiota. Probiotic supplementation has been reported to reduce liver injury; however, it is unclear whether enteropathogen infection exacerbates liver injury. The purpose of this study was to address this unanswered question using a rat model.
  
  
  METHODS
  Oral supplementation with Salmonella enterica serovar enteritidis (S. enteritidis) was given to rats for 7 days. Different degrees of acute liver injury were then induced by intraperitoneal injection of D-galactosamine. The presence and extent of liver injury was assayed by measuring the concentrations of serum alanine aminotransferase, aspartate aminotransferase, and total bilirubin. Histology was used to observe liver tissue damage. Additionally, we measured the changes in plasma endotoxin, serum cytokines and bacterial translocation to clarify the mechanisms underlying intestinal microbiota associated liver injury.
  
  
  RESULTS
  The levels of liver damage and endotoxin were significantly increased in the Salmonella infected rats with severe liver injury compared with the no infection rats with severe liver injury (P<0.01); The peyer's patch CD3+ T cell counts were increased significantly when the Salmonella infection with severe injury group was compared with the normal group (P<0.05). S. enteritidis pretreatment enhanced intestinal barrier impairment and bacterial translocation.
  
  
  CONCLUSIONS
  Oral S. enteritidis administration exacerbates acute liver injury, especially when injury was severe. Major factors of the exacerbation include inflammatory and oxidative stress injuries induced by the translocated bacteria and associated endotoxins, as well as over-activation of the immune system in the intestine and liver.
authors: State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, and Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China. ljli@zju.edu.cn.
authors: Yong-Tao
authors: YT
authors: Li
authors: Cheng-Bo
authors: CB
authors: Yu
authors: Dong
authors: D
authors: Yan
authors: Jian-Rong
authors: JR
authors: Huang
authors: Lan-Juan
authors: LJ
authors: Li
mesh_terms: D000208:Acute Disease; D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D018988:Bacterial Translocation; D001663:Bilirubin / Q000097:blood; D015415:Biomarkers / Q000097:blood; D017252:CD3 Complex / Q000276:immunology; D056486:Chemical and Drug Induced Liver Injury / Q000097:blood / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D016207:Cytokines / Q000276:immunology; D004195:Disease Models, Animal; D004731:Endotoxins / Q000378:metabolism; D005688:Galactosamine; D054884:Host-Pathogen Interactions; D008099:Liver / Q000378:metabolism / Q000382:microbiology* / Q000473:pathology; D008297:Male; D010581:Peyer's Patches / Q000276:immunology / Q000382:microbiology; D017207:Rats, Sprague-Dawley; D012480:Salmonella Infections / Q000097:blood / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D012477:Salmonella enteritidis / Q000276:immunology / Q000378:metabolism / Q000472:pathogenicity*; D013601:T-Lymphocytes / Q000276:immunology / Q000382:microbiology; D013997:Time Factors
chemical_list: D015415:Biomarkers; D017252:CD3 Complex; D016207:Cytokines; D004731:Endotoxins; D005688:Galactosamine; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D001663:Bilirubin