期刊
BRAIN BEHAVIOR AND IMMUNITY
卷 70, 期 -, 页码 48-60出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbi.2018.02.005
关键词
Parkinson's disease; Microbial dysbiosis; Gut-brain axis; Short-chain fatty acids; Glia; Neuroinflammation; Neurotransmitter; TLR4/TNF-alpha signaling
资金
- National Natural Science Foundation of China - China [81650007, 81771384]
- Jiangsu Double Innovation Plan of China - China [2014-27]
- Fundamental Research Funds for the Central Universities of China - China [JUSRP51619B]
- Jiangsu Six Peaks Project of China - China [2013-SWYY-041]
Parkinson's disease (PD) patients display alterations in gut microbiota composition. However, mechanism between gut microbial dysbiosis and pathogenesis of PD remains unexplored, and no recognized therapies are available to halt or slow progression of PD. Here we identified that gut microbiota from PD mice induced motor impairment and striatal neurotransmitter decrease on normal mice. Sequencing of 16S rRNA revealed that phylum Firmicutes and order Clostridiales decreased, while phylum Proteobacteria, order Turicibacterales and Enterobacteriales increased in fecal samples of PD mice, along with increased fecal short-chain fatty acids (SCFAs). Remarkably, fecal microbiota transplantation (FMT) reduced gut microbial dysbiosis, decreased fecal SCFAs, alleviated physical impairment, and increased striatal DA and 5-HT content of PD mice. Further, FMT reduced the activation of microglia and astrocytes in the substantia nigra, and reduced expression of TLRII/TNF-alpha signaling pathway components in gut and brain. Our study demonstrates that gut microbial dysbiosis is involved in PD pathogenesis, and FMT can protect PD mice by suppressing neuroinflammation and reducing TLR4/TNF-alpha signaling. (C) 2018 Elsevier Inc. All rights reserved.
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