The extracellular vesicle of depressive patient-derived Escherichia fergusonii induces vagus nerve-mediated neuroinflammation in mice

Bibliographic Details
Title: The extracellular vesicle of depressive patient-derived Escherichia fergusonii induces vagus nerve-mediated neuroinflammation in mice
Authors: Xiaoyang Ma, Hee-Seo Park, Yoon-Jung Shin, Jeon-Kyung Kim, Jung Kyung Hong, Seung-Won Han, In-Young Yoon, Dong-Hyun Kim
Source: Journal of Neuroinflammation, Vol 21, Iss 1, Pp 1-16 (2024)
Publisher Information: BMC, 2024.
Publication Year: 2024
Collection: LCC:Neurology. Diseases of the nervous system
Subject Terms: Gut dysbiosis, Depression, Escherichia fergusonii, Enterococcus faecium, Vagus nerve, Neurology. Diseases of the nervous system, RC346-429
More Details: Abstract Background Gut microbiota dysbiosis is closely associated with psychiatric disorders such as depression and anxiety (DA). In our preliminary study, fecal microbiota transplantation from volunteers with psychological stress and subclinical symptoms of depression (Vsd) induced DA-like behaviors in mice. Escherichia fergusonii (Esf) was found to be more abundant in the feces of Vsd compared to healthy volunteers. Therefore, we investigated the effect of Esf on DA-like behavior and neuroinflammation in mice with and without celiac vagotomy. Methods and results Orally gavaged Esf increased DA-like behaviors, tumor necrosis factor (TNF)-α, and toll-like receptor-4 (TLR4) expression, and NF-κB+Iba1+ and lipopolysaccharide (LPS)+Iba1+ cell populations, while decreasing serotonin, 5-HT1A receptor, and brain-derived neurotrophic factor (BDNF) expression in the hippocampus and prefrontal cortex. However, celiac vagotomy attenuated Esf-induced DA-like behavior and neuroinflammation. Orally gavaged extracellular vesicle (EV) from Vsd feces (vfEV) or Esf culture (esEV) induced DA-like behavior and inflammation in hippocampus, prefrontal cortex and colon. However, celiac vagotomy attenuated vfEV- or esEV-induced DA-like behaviors and inflammation in the brain alone, while vfEV- or esEV-induced blood LPS and TNF-α levels, colonic TNF-α expression and NF-κB-positive cell number, and fecal LPS level were not. Although orally gavaged fluorescence isothiocyanate-labeled esEV was translocated into the blood and hippocampus, celiac vagotomy decreased its translocation into the hippocampus alone. Conclusions esEVs may be translocated into the brain via the vagus nerve and bloodstream, subsequently inducing TNF-α expression and suppressing serotonin, its receptor, and BDNF expression through the activation of TLR4-mediated NF-κB signaling, thereby contributing to DA pathogenesis.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 1742-2094
Relation: https://doaj.org/toc/1742-2094
DOI: 10.1186/s12974-024-03211-7
Access URL: https://doaj.org/article/1c31636a47784d8893f4c15ef2e3eebf
Accession Number: edsdoj.1c31636a47784d8893f4c15ef2e3eebf
Database: Directory of Open Access Journals
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More Details
ISSN:17422094
DOI:10.1186/s12974-024-03211-7
Published in:Journal of Neuroinflammation
Language:English