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Front. Cell. Infect. Microbiol. | doi: 10.3389/fcimb.2018.00049

Triclosan enhances the clearing of pathogenic intracellular Salmonella or Candida albicans but disturbs the intestinal microbiota through mTOR-independent autophagy

Chao Wang1, Zhongyang Yu2, Xiaochen Shi1, Xudong Tang3,  Yang Wang1, Xueyan Wang3,  Yanan An1, Shulin Li1, Yan Li1, Xuefei Wang1, Wenjing Luan1, Zhaobin Chen4,  Mingyuan Liu1 and  LU YU1*
  • 1Jilin University, China
  • 2Renmin Hospital of Wuhan University, China
  • 3Research Institute of Tsinghua University in Shenzhen, China
  • 4Sichuan University, China

Triclosan (TCS) is a broad-spectrum antimicrobial agent, whose well-known antibacterial mechanism is inhibiting lipid synthesis. Autophagy, an innate immune response, is an intracellular process that delivers the cargo including pathogens to lysosomes for degradation. In this study, we first demonstrated that TCS induced autophagy in a dose-dependent manner in nonphagocytic cells (HeLa) and in macrophages (Raw264.7) and in vivo. The western blot results also revealed that TCS induced autophagy via the AMPK/ULK1 and JNK/ERK/p38 pathways independent of mTOR. The immunofluorescence results indicated that TCS up-regulated the expression of the ubiquitin receptors NDP52 and p62 and strengthened the colocalization of these receptors with Salmonella enterica Typhimurium (S. typhimurium) or Candida albicans (C. albicans) in infected MФ cells. In addition, sub-lethal concentrations of TCS enhanced the clearing of the pathogens S. typhimurium or C. albicans in infected MФ and in corresponding mouse infection models in vivo. Specifically, we found that a sub-inhibitory concentration of TCS induced autophagy, leading to an imbalance of the intestinal microflora in mice through the analysis of 16s rRNA Sequencing. Together, these results demonstrated that TCS induced autophagy, which enhanced the killing against pathogenic S. typhimurium or C. albicans within mammal cells but broke the balance of the intestinal microflora.

Keywords: Triclosan, Autophagy, mTOR-Independent, macrophage, antimicrobial

Received: 17 Aug 2017; Accepted: 09 Feb 2018.

Edited by:

Till Strowig, Helmholtz-Zentrum für Infektionsforschung, Germany

Reviewed by:

Paras K. Anand, Imperial College London, United Kingdom
Susan M. Bueno, Pontificia Universidad Católica de Chile, Chile  

Copyright: © 2018 Wang, Yu, Shi, Tang, Wang, Wang, An, Li, Li, Wang, Luan, Chen, Liu and YU. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Prof. LU YU, Jilin University, Changchun, China, yu_lu@jlu.edu.cn