Comorbidity between depression and inflammatory bowel disease explained by immune-inflammatory, oxidative, and nitrosative stress; tryptophan catabolite; and gut–brain pathways Martin-Subero,M, Anderson,G, Kanchanatawan,B, Berk,M and Maes,M 2016, Comorbidity between depression and inflammatory bowel disease explained by immune-inflammatory, oxidative, and nitrosative stress; tryptophan catabolite; and gut–brain pathways, CNS Spectrums, vol. 21, no. 2, pp. 184-198, doi: 10.1017/S1092852915000449. Attached Files Name Description MIMEType Size Downloads Title Comorbidity between depression and inflammatory bowel disease explained by immune-inflammatory, oxidative, and nitrosative stress; tryptophan catabolite; and gut–brain pathways Author(s) Martin-Subero,M Anderson,G Kanchanatawan,B Berk,M orcid.org/0000-0002-5554-6946 Maes,M Journal name CNS Spectrums Volume number 21 Issue number 2 Start page 184 End page 198 Total pages 15 Publisher Cambridge University Press Place of publication Cambridge, Eng. Publication date 2016-04-01 ISSN 1092-8529 Keyword(s) Comorbidity haptoglobin immunology inflammatory bowel disease major depression oxidative stress Science & Technology Life Sciences & Biomedicine Clinical Neurology Psychiatry Neurosciences & Neurology SYSTEMIC-LUPUS-ERYTHEMATOSUS SOLUBLE INTERLEUKIN-2 RECEPTORS CHRONIC-FATIGUE-SYNDROME ACUTE-PHASE PROTEINS C-REACTIVE PROTEIN CROHNS-DISEASE ULCERATIVE-COLITIS INDOLEAMINE 2,3-DIOXYGENASE BACTERIAL TRANSLOCATION Summary 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. Language eng DOI 10.1017/S1092852915000449 Field of Research 119999 Medical and Health Sciences not elsewhere classified 110319 Psychiatry (incl Psychotherapy) 111714 Mental Health 1103 Clinical Sciences 1109 Neurosciences Socio Economic Objective 929999 Health not elsewhere classified HERDC Research category C1 Refereed article in a scholarly journal ERA Research output type C Journal article Copyright notice ©2016 Cambridge University Press Persistent URL http://hdl.handle.net/10536/DRO/DU:30078426 Document type: Journal Article Collections: Faculty of Health School of Medicine Related Links Link Description Connect to published version Go to link with your DU access privileges     Unless expressly stated otherwise, the copyright for items in DRO is owned by the author, with all rights reserved. Versions Version Filter Type Thu, 24 Sep 2015, 12:51:57 EST Fri, 25 Sep 2015, 05:00:43 EST Fri, 25 Sep 2015, 06:12:34 EST Tue, 06 Oct 2015, 11:12:22 EST Tue, 06 Oct 2015, 11:16:37 EST Mon, 18 Jul 2016, 15:44:50 EST Tue, 26 Jul 2016, 12:23:11 EST Fri, 29 Jul 2016, 12:34:02 EST Wed, 12 Oct 2016, 14:06:27 EST Wed, 01 Mar 2017, 07:21:42 EST Sun, 10 Nov 2019, 14:37:50 EST Thu, 25 Feb 2021, 00:35:42 EST Filtered Full Citation counts:   Cited 90 times in TR Web of Science Cited 95 times in Scopus Search Google Scholar Access Statistics: 558 Abstract Views, 2 File Downloads  -  Detailed Statistics Created: Thu, 24 Sep 2015, 12:51:57 EST

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