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J Neuroimmunol. 2017 Dec 15;313:92-98. doi: 10.1016/j.jneuroim.2017.10.016. Epub 2017 Oct 28.

Inflammation-induced depression: Its pathophysiology and therapeutic implications.

Author information

1
Department of Psychiatry, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea.
2
Department of Psychiatry, College of Medicine, Korea University, Ansan Hospital, Ansan, Republic of Korea. Electronic address: yongku@korea.edu.

Abstract

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.

KEYWORDS:

Depression; Immunopharmacology; Inflammation; Kynurenine pathway; Tryptophan

PMID:
29153615
DOI:
10.1016/j.jneuroim.2017.10.016
[Indexed for MEDLINE]

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