The administration of Escherichia coli Nissle 1917 ameliorates irinotecan–induced intestinal barrier dysfunction and gut microbial dysbiosis in mice

大肠杆菌 失调 微生物学 肠道菌群 伊立替康 肠道菌群 药理学 生物 免疫学 化学 医学 细菌 内科学 生物化学 结直肠癌 癌症 遗传学 基因
作者
Yurong Wang,Lie Sun,Shanwen Chen,Shihao Guo,Taohua Yue,Qisheng Hou,Mei Feng,Hao Xu,Yucun Liu,Pengyuan Wang,Yisheng Pan
出处
期刊:Life Sciences [Elsevier BV]
卷期号:231: 116529-116529 被引量:51
标识
DOI:10.1016/j.lfs.2019.06.004
摘要

The present study investigated the effect of Escherichia coli Nissle 1917 (EcN) on irinotecan-induced intestinal barrier dysfunction and gut microbial dysbiosis in a mouse model and in the human colonic cells lines Caco-2.Male BALB/c mice received irinotecan intraperitoneal injection with or without EcN administration intragastrically. Body weight, diarrhea severity, intestinal permeability and histopathological analysis of ileum epithelia of mice from different groups were assessed. The expression and localization of tight junction proteins were examined using western blot and immunofluorescence. Gut microbiota structure and diversity were measured with 16 S rRNA sequencing. Caco-2 monolayers were incubated with EcN culture supernatant (EcNsup) or SN-38 and the monolayer barrier function was assessed by transepithelial electrical resistance (TER) and FITC-dextran 4000 Da (FD-4) flux.Pretreatment with EcN significantly attenuated irinotecan-induced weight loss and diarrhea in mice. In addition, EcN inhibited the increased intestinal permeability and decreased Claudin-1 expression in irinotecan-treated mice. Furthermore, irinotecan treatment decreased the diversity of gut microbiota and increased the relative abundance of Proteobacteria compared to control group. EcN administration ameliorated the gut microbiota dysbiosis. In Caco-2 monolayers, EcNsup ameliorated the decreased TER and increased FD-4 flux elicited by SN-38. Moreover, EcNsup attenuated SN-38-induced altered localization and distribution of Claudin-1 in Caco-2 monolayers.Our results indicated that the administration of EcN protected against irinotecan-induced intestinal injury by regulating intestinal barrier function and gut microbiota.
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