Format

Send to:

Choose Destination
See comment in PubMed Commons below
CNS Neurosci Ther. 2014 Feb;20(2):119-24. doi: 10.1111/cns.12170. Epub 2013 Nov 27.

Involvement of inflammasome activation in lipopolysaccharide-induced mice depressive-like behaviors.

Author information

  • 1Laboratory of Stress Medicine, Faculty of Psychology and Mental Health, Second Military Medical University, Shanghai, China.

Abstract

AIMS:

The NLRP3 inflammasome is a cytoplasmic multiprotein complex of the innate immune system that regulates the cleavage of interleukin-1β and interleukin-18 precursors. It can detect a wide range of danger signals and trigger a series of immune-inflammatory reactions. There were plenty of studies indicating that activation of the immune system played pivotal roles in depression. However, the underlying mechanisms of immune-depression interactions remained elusive and there was no report about the involvement of inflammasome activation in depression.

METHODS:

We established an acute depression mouse model with lipopolysaccharide to explore the involvement of inflammasome activation in depression.

RESULTS:

The lipopolysaccharide-treated mice displayed depressive-like behaviors and pro-inflammatory cytokine interleukin-1β protein and mRNA levels significantly increased. The NLRP3 inflammasome mRNA expression level also significantly elevated in depressed mice brain. Pretreatment with the NLRP3 inflammasome inhibitor Ac-YVAD-CMK significantly abrogated the depressive-like behaviors induced by lipopolysaccharide.

CONCLUSION:

These data suggest for the first time that the NLRP3 inflammasome is involved in lipopolysaccharide-induced mice depressive-like behaviors. The NLRP3 inflammasome may be a central mediator between immune activation and depression, which raises the possibility that it may be a more specific target for the depression treatments in the near future.

© 2013 John Wiley & Sons Ltd.

KEYWORDS:

Cytokines; Depression; Inflammation; Interleukin-1β; NLRP3 inflammasome

PMID:
24279434
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Blackwell Publishing
    Loading ...
    Write to the Help Desk