title: Lactobacillus plantarum prevents bacterial translocation in rats following ischemia and reperfusion injury.
abstract: BACKGROUND
  Bacterial translocation is considered a major cause of initiation and development of systemic sepsis and multiple organ dysfunction in clinic. The aim of this study was to determine the ability of a defined Lactobacillus plantarum to prevent ischemia/reperfusion (I/R) induced intestinal infection.
  
  
  METHODS
  Female Sprague-Dawley rats were randomly allocated into three groups: (1) controls (sham-operated, no treatment), (2) ischemia/reperfusion and (3) ischemia/reperfusion and Lactobacillus plantarum treatment. Lactobacillus plantarum L2 was administered daily intragastrically 14 days prior to induction of I/R. Rats were then sacrificed, and tissue and blood samples were cultured to determine bacterial translocation. Cytokines in plasma were detected by ELISA. Ileal segments were removed for morphological examination.
  
  
  RESULTS
  Intestinal I/R induced excess pro-inflammatory cytokine secretion and barrier dysfunction (increased epithelial cell apoptosis, cecal flora dysbiosis, disruption of mucosa and multiple erosions) in the intestine, associated with increased bacterial translocation to extraintestinal sites. Approximately 87.5% of rats exposed to I/R had bacterial translocation while there was no bacterial translocation in controls. However, pretreatment of animals with Lactobacillus plantarum completely prevented I/R induced bacterial translocation, reduced pro-inflammatory cytokine release, and intestinal epithelial cell apoptosis, resulting in recovered microflora and mucosal integrity.
  
  
  CONCLUSIONS
  These findings indicate that Lactobacillus plantarum L2 can prevent I/R-induced bacterial translocation and intestinal barrier dysfunction and, thereby, exert beneficial effects in the intestinal tract.
authors: Department of Surgery, Research Institute of General Surgery, Jin Ling Hospital, Nanjing, Jiangsu 210002, People's Republic of China.
authors: Bin
authors: B
authors: Wang
authors: Qian
authors: Q
authors: Huang
authors: Wei
authors: W
authors: Zhang
authors: Ning
authors: N
authors: Li
authors: Jieshou
authors: J
authors: Li
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