Tryptophan-kynurenine metabolism: a link between the gut and brain for depression in inflammatory bowel disease

Inflammatory bowel disease (IBD), which mainly includes ulcerative colitis (UC) and Crohn's disease (CD), is a group of chronic bowel diseases that are characterized by abdominal pain, diarrhea, and bloody stools. IBD is strongly associated with depression, and its patients have a higher incidence of depression than the general population. Depression also adversely affects the quality of life and disease prognosis of patients with IBD. The tryptophan-kynurenine metabolic pathway degrades more than 90% of tryptophan (TRP) throughout the body, with indoleamine 2,3-dioxygenase (IDO), the key metabolic enzyme, being activated in the inflammatory environment. A series of metabolites of the pathway are neurologically active, among which kynerunic acid (KYNA) and quinolinic acid (QUIN) are molecules of great interest in recent studies on the mechanisms of inflammation-induced depression. In this review, the relationship between depression in IBD and the tryptophan-kynurenine metabolic pathway is overviewed in the light of recent publications.

Automated summary

Inflammatory bowel disease (IBD) patients are at a higher risk of depression, which can negatively impact disease prognosis and quality of life. The key metabolic enzyme indoleamine 2,3-dioxygenase (IDO) in the tryptophan-kynurenine metabolic pathway is activated in the inflammatory environment, leading to potentially neurologically active metabolites associated with inflammation-induced depression.