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Pro-inflammatory cytokines: Potential links between the endocannabinoid system and the kynurenine pathway in depression

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisReviewForskningpeer review


  • Ferenc Zádor, Hungarian Academy of Sciences
  • ,
  • Sâmia Joca
  • Gábor Nagy-Grócz, University of Szeged
  • ,
  • Szabolcs Dvorácskó, Hungarian Academy of Sciences, University of Szeged
  • ,
  • Edina Szűcs, Hungarian Academy of Sciences, University of Szeged
  • ,
  • Csaba Tömböly, Hungarian Academy of Sciences
  • ,
  • Sándor Benyhe, Hungarian Academy of Sciences
  • ,
  • László Vécsei, University of Szeged

Substance use/abuse is one of the main causes of depressive symptoms. Cannabis and synthetic cannabinoids in particular gained significant popularity in the past years. There is an increasing amount of clinical data associating such compounds with the inflammatory component of depression, indicated by the up-regulation of pro-inflammatory cytokines. Pro-inflammatory cyto-kines are also well-known to regulate the enzymes of the kynurenine pathway (KP), which is responsible for metabolizing tryptophan, a precursor in serotonin synthesis. Enhanced pro-inflam-matory cytokine levels may over-activate the KP, leading to tryptophan depletion and reduced ser-otonin levels, which can subsequently precipitate depressive symptoms. Therefore, such mechanism might represent a possible link between the endocannabinoid system (ECS) and the KP in depression, via the inflammatory and dysregulated serotonergic component of the disorder. This review will summarize the data regarding those natural and synthetic cannabinoids that increase pro-inflammatory cytokines. Furthermore, the data on such cytokines associated with KP activation will be further reviewed accordingly. The interaction of the ECS and the KP has been postulated and demonstrated in some studies previously. This review will further contribute to this yet less explored connection and propose the KP to be the missing link between cannabinoid-induced inflammation and depressive symptoms.

TidsskriftInternational Journal of Molecular Sciences
StatusUdgivet - jun. 2021

Bibliografisk note

Funding Information:
Funding: G.N.-G. was supported by the ÚNKP-20-4 New National Excellence Program of the Ministry for Innovation and Technology from the source of the National Research, Development and Innovation Fund. S.J. is supported by the Aarhus University Research Foundation (AUFF starting grant) and FAPESP (17/24304-0). This research was supported by the EU-funded Hungarian grant EFOP-3.6.1-16-2016-00008 and by the TUDFO/47138-1/2019-ITM, GINOP 2.3.2-15-2016-00034.

Publisher Copyright:
© 2021 by the authors. Licensee MDPI, Basel, Switzer-land.

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