TY - JOUR
T1 - Inflammation-induced depression
T2 - Its pathophysiology and therapeutic implications
AU - Jeon, Sang Won
AU - Kim, Yong Ku
N1 - 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.
PY - 2017/12/15
Y1 - 2017/12/15
N2 - 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.
AB - 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.
KW - Depression
KW - Immunopharmacology
KW - Inflammation
KW - Kynurenine pathway
KW - Tryptophan
UR - http://www.scopus.com/inward/record.url?scp=85032689097&partnerID=8YFLogxK
U2 - 10.1016/j.jneuroim.2017.10.016
DO - 10.1016/j.jneuroim.2017.10.016
M3 - Review article
C2 - 29153615
AN - SCOPUS:85032689097
SN - 0165-5728
VL - 313
SP - 92
EP - 98
JO - Journal of Neuroimmunology
JF - Journal of Neuroimmunology
ER -