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NLRP3 Inflammasome Contributes to Lipopolysaccharide-induced Depressive-Like Behaviors via Indoleamine 2,3-dioxygenase Induction

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dc.contributor.author김철훈-
dc.contributor.author유제욱-
dc.contributor.author황인화-
dc.date.accessioned2018-07-20T08:34:11Z-
dc.date.available2018-07-20T08:34:11Z-
dc.date.issued2017-
dc.identifier.issn1461-1457-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/161292-
dc.description.abstractBackground: Inflammation may play a significant role in the pathogenesis of depression, although the molecular target for the treatment of inflammation-mediated depressive symptoms remains to be elucidated. Recent studies have implicated the NLRP3 inflammasome in various psychiatric disorders, including depression. However, the underlying mechanism by which NLRP3 inflammasome activation mediates the progression of depressive-like behaviors remains poorly understood. Methods: We examined whether NLRP3 deficiency influenced depressive-like behaviors and cerebral inflammation following systemic administration of lipopolysaccharide in mice. To further assess the contribution of the NLRP3 inflammasome to the progression of depression, we evaluated the effects of NLRP3 signaling on levels of indoleamine 2,3-dioxygenase. Results: Nlrp3-deficient mice exhibited significant attenuation of depressive-like behaviors and cerebral caspase-1 activation in a lipopolysaccharide-induced model of depression. Treatment with the antidepressant amitriptyline failed to block NLRP3-dependent activation of caspase-1, but inhibited lipopolysaccharide-promoted production of interleukin-1β mRNA via suppressing NF-κB signaling in mouse mixed glial cultures. Interestingly, lipopolysaccharide administration produced NLRP3-dependent increases in indoleamine 2,3-dioxygenase expression and activity of mouse brain. Furthermore, inflammasome-activating stimulations, but not treatment with the inflammasome product interleukin-1β, triggered indoleamine 2,3-dioxygenase mRNA induction in mixed glial cells. Conclusions: Our data indicate that the NLRP3 inflammasome is significantly implicated in the progression of systemic inflammation-induced depression. NLRP3-dependent caspase-1 activation produced significant increases in indoleamine 2,3-dioxygenase levels, which may play a significant role in lipopolysaccharide-induced depression. Collectively, our findings suggest that indoleamine 2,3-dioxygenase is a potential downstream mediator of the NLRP3 inflammasome in inflammation-mediated depressive-like behaviors.-
dc.description.statementOfResponsibilityopen-
dc.languageEnglish-
dc.publisherOxford Oxford University Press-
dc.relation.isPartOfINTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rightshttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleNLRP3 Inflammasome Contributes to Lipopolysaccharide-induced Depressive-Like Behaviors via Indoleamine 2,3-dioxygenase Induction-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine-
dc.contributor.departmentDept. of Pharmacology-
dc.contributor.googleauthorSeon-A Jeon-
dc.contributor.googleauthorEunju Lee-
dc.contributor.googleauthorInhwa Hwang-
dc.contributor.googleauthorBoyoung Han-
dc.contributor.googleauthorSangjun Park-
dc.contributor.googleauthorSeunghwan Son-
dc.contributor.googleauthorJungmin Yang-
dc.contributor.googleauthorSujeong Hong-
dc.contributor.googleauthorChul Hoon Kim-
dc.contributor.googleauthorJunghyun Son-
dc.contributor.googleauthorJe-Wook Yu-
dc.identifier.doi10.1093/ijnp/pyx065-
dc.contributor.localIdA01057-
dc.contributor.localIdA02508-
dc.contributor.localIdA05445-
dc.relation.journalcodeJ01135-
dc.identifier.eissn1469-5111-
dc.identifier.pmid29016824-
dc.subject.keywordNLRP3 inflammasome-
dc.subject.keyworddepression-
dc.subject.keywordindoleamine 2,3-dioxygenase-
dc.contributor.alternativeNameKim, Chul Hoon-
dc.contributor.alternativeNameYu, Je Wook-
dc.contributor.alternativeNameHwang, Inhwa-
dc.contributor.affiliatedAuthorKim, Chul Hoon-
dc.contributor.affiliatedAuthorYu, Je Wook-
dc.contributor.affiliatedAuthorHwang, Inhwa-
dc.citation.volume20-
dc.citation.number11-
dc.citation.startPage896-
dc.citation.endPage906-
dc.identifier.bibliographicCitationINTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY, Vol.20(11) : 896-906, 2017-
dc.identifier.rimsid61214-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Microbiology (미생물학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Pharmacology (약리학교실) > 1. Journal Papers

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