Inflammation-induced depression: Its pathophysiology and therapeutic implications

Sang Won Jeon, Yong Ku Kim

    Research output: Contribution to journalReview articlepeer-review

    101 Citations (Scopus)


    Inflammation is not the only cause of depression and cannot explain its entire pathophysiology, but it is an important pathogenic factor that explains one possible mechanism of depression, with the kynurenine (KYN) pathway of tryptophan at its center. In particular, greater impairment seems to exist in the KYN pathway in inflammation-induced depression related to immunotherapy, autoimmune disease, and infection. In patients with these conditions, immunopharmacology is likely to be an important therapy. To develop this therapy, clear evidence of the immune-KYN pathway must be established via multiple types of experiments. This paper reviews the body of evidence, not only for the action of tryptophan (TRY) and consequent serotonin depletion, but also for the detrimental effects of TRY catabolites and the key enzymes in the KYN pathway that play important roles in the pathophysiology of inflammation-induced depression. In addition, this paper explores a potential treatment strategy for inflammation-induced depression using KYN metabolism.

    Original languageEnglish
    Pages (from-to)92-98
    Number of pages7
    JournalJournal of Neuroimmunology
    Publication statusPublished - 2017 Dec 15

    Bibliographical note

    Funding Information:
    This research was supported by a grant from the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea ( HC15C1405 ).

    Publisher Copyright:
    © 2017 Elsevier B.V.


    • Depression
    • Immunopharmacology
    • Inflammation
    • Kynurenine pathway
    • Tryptophan

    ASJC Scopus subject areas

    • Immunology and Allergy
    • Immunology
    • Neurology
    • Clinical Neurology


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