Kinetics and protective role of autophagy in a mouse cecal ligation and puncture-induced sepsis View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2013-07-24

AUTHORS

Waka Takahashi, Eizo Watanabe, Lisa Fujimura, Haruko Watanabe-Takano, Hiroyuki Yoshidome, Paul E Swanson, Takeshi Tokuhisa, Shigeto Oda, Masahiko Hatano

ABSTRACT

IntroductionIt is not well understood whether the process of autophagy is accelerated or blocked in sepsis, and whether it is beneficial or harmful to the immune defense mechanism over a time course during sepsis. Our aim was to determine both the kinetics and the role of autophagy in sepsis.MethodsWe examined autophagosome and autolysosome formation in a cecal ligation and puncture (CLP) mouse model of sepsis (in C57BL/6N mice and GFP-LC3 transgenic mice), using western blotting, immunofluorescence, and electron microscopy. We also investigated the effect of chloroquine inhibition of autophagy on these processes.ResultsAutophagy, as demonstrated by increased LC3-II/LC3-I ratios, is induced in the liver, heart, and spleen over 24 h after CLP. In the liver, autophagosome formation peaks at 6 h and declines by 24 h. Immunofluorescent localization of GFP-LC3 dots (alone and with lysosome-associated membrane protein type 1 (LAMP1)), as well as electron microscopic examination, demonstrate that both autophagosomes and autolysosomes are increased after CLP, suggesting that intact autophagy mechanisms operate in the liver in this model. Furthermore, inhibition of autophagy process by chloroquine administration immediately after CLP resulted in elevated serum transaminase levels and a significant increase in mortality.ConclusionsAll autophagy-related processes are properly activated in the liver in a mouse model of sepsis; autophagy appears to play a protective role in septic animals. More... »

PAGES

r160

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/cc12839

DOI

http://dx.doi.org/10.1186/cc12839

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1026367293

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/23883625


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