title: Bifidobacteria may be beneficial to intestinal microbiota and reduction of bacterial translocation in mice following ischaemia and reperfusion injury.
abstract: The aim of the present study was to determine the effect of peroral bifidobacteria on the intestinal microbiota, barrier function and bacterial translocation (BT) in a mouse model of ischaemia and reperfusion (I/R) injury. A total of twenty-four male BALB/c mice were randomly allocated into three groups: (1) sham-operated, (2) I/R and (3) I/R injury and bifidobacteria pretreatment (109 colony-forming units/d). Bifidobacteria were administered daily intragastrically for 2 weeks before induction of I/R. Subsequently, samples of caecal content, intestinal mucosa, ileal segments, blood, mesenteric lymph nodes (MLN) and distant organs (liver, spleen and kidney) were prepared for examination. In the I/R model, barrier dysfunction (caecal microbiota dysbiosis, disruption of tight junction (TJ), increased epithelial cell apoptosis, disruption of mucosa and multiple erosions) in the intestine was observed, associated with increased BT to extraintestinal sites. The ratio of BT to MLN and distant organs in mice exposed to I/R injury was 62·5 %, which was significantly higher than the sham-operated group. However, pretreatment of animals with bifidobacteria prevented I/R-induced BT, reduced pro-inflammatory cytokine release, the levels of endotoxin, intestinal epithelial cell apoptosis, disruption of TJ and increased the concentration of SCFA, resulting in recovered microbiota and mucosal integrity. Bifidobacteria may be beneficial in reducing BT in I/R injury of mice. Therefore, peroral administration of bifidobacteria is a potential strategy to prevent I/R-induced BT and intestinal barrier dysfunction.
authors.affiliation: Department of General Surgery, Jinling Hospital, Medical School of Nanjing University, No. 305 East Zhongshan Road, Nanjing, People's Republic of China.
authors.forename: Honggang
authors.initials: H
authors.lastname: Wang
authors.forename: Wei
authors.initials: W
authors.lastname: Zhang
authors.forename: Lugen
authors.initials: L
authors.lastname: Zuo
authors.forename: Weiming
authors.initials: W
authors.lastname: Zhu
authors.forename: Bin
authors.initials: B
authors.lastname: Wang
authors.forename: Qiurong
authors.initials: Q
authors.lastname: Li
authors.forename: Jieshou
authors.initials: J
authors.lastname: Li
mesh_terms: D000818:Animals; D018988:Bacterial Translocation; D001644:Bifidobacterium / Q000502:physiology*; D004731:Endotoxins; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D007422:Intestines / Q000382:microbiology* / Q000473:pathology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D011897:Random Allocation; D015427:Reperfusion Injury / Q000378:metabolism* / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: D004731:Endotoxins; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha