Open AccessInvolvement of Inflammasome Activation in Lipopolysaccharide‐induced Mice Depressive‐like Behaviors
Author(s) -
Zhang Yi,
Liu Lei,
Peng YunLi,
Liu YunZi,
Wu TengYun,
Shen XiaoLiang,
Zhou JiangRui,
Sun DingYa,
Huang AiJun,
Wang Xia,
Wang YunXia,
Jiang ChunLei
Publication year - 2014
Publication title -
cns neuroscience and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 69
eISSN - 1755-5949
pISSN - 1755-5930
DOI - 10.1111/cns.12170
Subject(s) - inflammasome , lipopolysaccharide , immune system , mediator , innate immune system , cytokine , interleukin , tumor necrosis factor alpha , inflammation , immunology , microbiology and biotechnology , medicine , biology
Summary Aims The NLRP 3 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 m RNA levels significantly increased. The NLRP 3 inflammasome m RNA expression level also significantly elevated in depressed mice brain. Pretreatment with the NLRP 3 inflammasome inhibitor A c‐ YVAD ‐ CMK significantly abrogated the depressive‐like behaviors induced by lipopolysaccharide. Conclusion These data suggest for the first time that the NLRP 3 inflammasome is involved in lipopolysaccharide‐induced mice depressive‐like behaviors. The NLRP 3 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.