4.3 Article

Intestinal dysbacteriosis contributes to decreased intestinal mucosal barrier function and increased bacterial translocation

期刊

LETTERS IN APPLIED MICROBIOLOGY
卷 58, 期 4, 页码 384-392

出版社

WILEY
DOI: 10.1111/lam.12201

关键词

bacterial translocation; dysbacteriosis; colistin; barrier dysfunction

资金

  1. National Ministry of Health for the Digestive Disease [201002020]
  2. National Science Foundation of China [30830098, 81200263, 30972881, 81170365]
  3. Model Animal Research Center, Nanjing University (Nanjing, China)

向作者/读者索取更多资源

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 7days, 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. Significance and Impact of the Study 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.

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