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NLRP3 Inflammasome Is Critical for Lipopolysaccharide‐Induced Depressive‐Like Behaviors
Author(s) -
Lee Eunju,
Jeon SeonA,
Hwang Inhwa,
Yu JeWook
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.lb193
Subject(s) - inflammasome , proinflammatory cytokine , lipopolysaccharide , mediator , inflammation , caspase 1 , hippocampus , pathogenesis , medicine , interleukin , immunology , cytokine
Cerebral inflammation is considered to contribute to the pathogenesis of depressive disorders, but the molecular target to intervene inflammation‐mediated depressive symptoms is still poorly elucidated. Recent studies intriguingly proposed the implication of NLRP3 inflammasome signaling in the depressive‐like disorders, although the molecular basis by which NLRP3 inflammasome activation contributes to depression is unclear. In this study, we examined lipopolysaccharide (LPS)‐induced depressive‐like behaviors in wild‐type and Nlrp3‐deficient mice. The levels of proinflammatory cytokines in the brain homogenate were not significantly different between wild‐type and Nlrp3‐deficient mice after LPS administration. However, significant reduction of active caspase‐1 was observed in the hippocampus of Nlrp3‐deficient mice brain compared to wild‐type mice. Of interest, LPS administration to mice caused a cerebral induction of Ido mRNA in a NLRP3‐dependent manner. Supporting this data, NLRP3 inflammasome‐activating stimulations, but not interleukin‐1β treatment, triggered a significant induction of IDO in mixed glial cells. Collectively, our findings suggest that IDO is a potential downstream mediator of the NLRP3 inflammasome in the progression of depressive‐like behaviors. Support or Funding Information This work was supported by the Bio & Medical Technology Development Program of the NRF funded by the Korean government, (2015M3A9B6073856)