title: Intestinal dysbacteriosis contributes to decreased intestinal mucosal barrier function and increased bacterial translocation.
abstract: The purpose of this study was to determine the effect of colistin-induced intestinal dysbacteriosis on intestinal mucosal barrier function and bacterial translocation in a mouse model. Colistin or saline was administered orally for 7 days, and populations of viable organisms from the caecal mucosa and its content, the ileal segments, the mesenteric lymph nodes (MLNs) and the internal organs were prepared for examination. In the intestinal dysbacteriosis model, intestinal barrier dysfunction was observed and associated with increased bacterial translocation to extraintestinal sites. The extent of bacterial translocation to the MLNs and internal organs in the colistin group was significantly higher than in the saline group. Colistin-induced intestinal dysbacteriosis was shown to injure the intestinal mucosa barrier function and increase bacterial dislocation.
  
  
  CONCLUSIONS
  Colistin has been reported to be effective in selective digestive decontamination (SDD), which is an infection prevention measure used in the treatment of certain patients in intensive care. We are the first to report that colistin-induced intestinal dysbacteriosis can injure intestinal mucosal barrier function and increase bacterial translocation, whereas a high dose of colistin does not damage the intestinal mucosal barrier in germ-free (GF) mice raised in a GF environment. These results may indicate that prolonged use of a high dose of a SDD medication should be carefully considered.
authors.affiliation: Department of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing, Jiangsu Province, China.
authors.forename: H
authors.initials: H
authors.lastname: Wang
authors.forename: W
authors.initials: W
authors.lastname: Zhang
authors.forename: L
authors.initials: L
authors.lastname: Zuo
authors.forename: J
authors.initials: J
authors.lastname: Dong
authors.forename: W
authors.initials: W
authors.lastname: Zhu
authors.forename: Y
authors.initials: Y
authors.lastname: Li
authors.forename: L
authors.initials: L
authors.lastname: Gu
authors.forename: J
authors.initials: J
authors.lastname: Gong
authors.forename: Q
authors.initials: Q
authors.lastname: Li
authors.forename: N
authors.initials: N
authors.lastname: Li
authors.forename: J
authors.initials: J
authors.lastname: Li
mesh_terms: D000818:Animals; D000900:Anti-Bacterial Agents; D018988:Bacterial Translocation / Q000187:drug effects; D002432:Cecum / Q000382:microbiology; D003091:Colistin; D064806:Dysbiosis / Q000139:chemically induced / Q000382:microbiology* / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D007413:Intestinal Mucosa / Q000382:microbiology* / Q000473:pathology / Q000503:physiopathology; D007422:Intestines / Q000382:microbiology; D008198:Lymph Nodes / Q000382:microbiology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D019108:Tight Junctions / Q000648:ultrastructure
chemical_list: D000900:Anti-Bacterial Agents; D003091:Colistin
keywords: bacterial translocation; barrier dysfunction; colistin; dysbacteriosis