title: Comorbidity between depression and inflammatory bowel disease explained by immune-inflammatory, oxidative, and nitrosative stress; tryptophan catabolite; and gut-brain pathways.
abstract: The nature of depression has recently been reconceptualized, being conceived as the clinical expression of activated immune-inflammatory, oxidative, and nitrosative stress (IO&NS) pathways, including tryptophan catabolite (TRYCAT), autoimmune, and gut-brain pathways. IO&NS pathways are similarly integral to the pathogenesis of inflammatory bowel disease (IBD). The increased depression prevalence in IBD associates with a lower quality of life and increased morbidity in IBD, highlighting the role of depression in modulating the pathophysiology of IBD.This review covers data within such a wider conceptualization that better explains the heightened co-occurrence of IBD and depression. Common IO&NS underpinning between both disorders is evidenced by increased pro-inflammatory cytokine levels, eg, interleukin-1 (IL-1) and tumor necrosis factor-α, IL-6 trans-signalling; Th-1- and Th-17-like responses; neopterin and soluble IL-2 receptor levels; positive acute phase reactants (haptoglobin and C-reactive protein); lowered levels of negative acute phase reactants (albumin, transferrin, zinc) and anti-inflammatory cytokines (IL-10 and transforming growth factor-β); increased O&NS with damage to lipids, proteinsm and DNA; increased production of nitric oxide (NO) and inducible NO synthase; lowered plasma tryptophan but increased TRYCAT levels; autoimmune responses; and increased bacterial translocation. As such, heightened IO&NS processes in depression overlap with the biological underpinnings of IBD, potentially explaining their increased co-occurrence. This supports the perspective that there is a spectrum of IO&NS disorders that includes depression, both as an emergent comorbidity and as a contributor to IO&NS processes. Such a frame of reference has treatment implications for IBD when "comorbid" with depression.
authors: 1Department of Psychiatry,Hospital Universitari Germans Trias I Pujol,Badalona,Spain.
authors: Marta
authors: M
authors: Martin-Subero
authors: 3Department of Psychiatry,CRC,Glasgow,UK.
authors: George
authors: G
authors: Anderson
authors: 4Department of Psychiatry, Faculty of Medicine,Chulalongkorn University,Bangkok,Thailand.
authors: Buranee
authors: B
authors: Kanchanatawan
authors: 5Department of Psychiatry,University of Melbourne,Parkville,Victoria,Australia.
authors: Michael
authors: M
authors: Berk
authors: 4Department of Psychiatry, Faculty of Medicine,Chulalongkorn University,Bangkok,Thailand.
authors: Michael
authors: M
authors: Maes
mesh_terms: D001921:Brain / Q000276:immunology* / Q000378:metabolism; D015897:Comorbidity; D003863:Depression / Q000453:epidemiology / Q000276:immunology* / Q000378:metabolism; D003866:Depressive Disorder / Q000453:epidemiology / Q000276:immunology* / Q000378:metabolism; D000069196:Gastrointestinal Microbiome / Q000276:immunology* / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000378:metabolism; D015212:Inflammatory Bowel Diseases / Q000453:epidemiology / Q000276:immunology* / Q000378:metabolism; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000276:immunology* / Q000382:microbiology; D015538:Nitrosation; D018384:Oxidative Stress / Q000276:immunology* / Q000502:physiology; D013312:Stress, Physiological / Q000276:immunology / Q000502:physiology; D014364:Tryptophan / Q000276:immunology / Q000378:metabolism
chemical_list: D014364:Tryptophan
keywords: Comorbidity; haptoglobin; immunology; inflammatory bowel disease; major depression; oxidative stress