Papers

Peer-reviewed Lead author
Sep, 2017

Exercise training enhances in vivo clearance of endotoxin and attenuates inflammatory responses by potentiating Kupffer cell phagocytosis

SCIENTIFIC REPORTS
  • Shoichi Komine
  • ,
  • Kentaro Akiyama
  • ,
  • Eiji Warabi
  • ,
  • Sechang Oh
  • ,
  • Keisuke Kuga
  • ,
  • Kazunori Ishige
  • ,
  • Shinji Togashi
  • ,
  • Toru Yanagawa
  • ,
  • Junichi Shoda

Volume
7
Number
1
First page
11977
Last page
Language
English
Publishing type
Research paper (scientific journal)
DOI
10.1038/s41598-017-12358-8
Publisher
NATURE PUBLISHING GROUP

The failure of Kupffer cells (KCs) to remove endotoxin is an important factor in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). In this study, the effects of exercise training on KC function were studied in terms of in vivo endotoxin clearance and inflammatory responses. Mice were allocated into rest and exercise groups. KC bead phagocytic capacity and plasma steroid hormone levels were determined following exercise training. Endotoxin and inflammatory cytokine levels in plasma were determined over time following endotoxin injection. KC bead phagocytic capacity was potentiated and clearance of exogenously-injected endotoxin was increased in the exercise group. Inflammatory cytokine (TNF-alpha and IL-6) levels were lower in the exercise group. We found that only DHEA was increased in the plasma of the exercise group. In an in vitro experiment, the addition of DHEA to RAW264.7 cells increased bead phagocytic capacity and attenuated endotoxin-induced inflammatory responses. These results suggest that exercise training modulates in vivo endotoxin clearance and inflammatory responses in association with increased DHEA production. These exercise-induced changes in KC capacity may contribute to a slowing of disease progression in NAFLD patients.

Link information
DOI
https://doi.org/10.1038/s41598-017-12358-8
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/28931917
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000411185100030&DestApp=WOS_CPL
ID information
  • DOI : 10.1038/s41598-017-12358-8
  • ISSN : 2045-2322
  • Pubmed ID : 28931917
  • Web of Science ID : WOS:000411185100030

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