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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.

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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
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
Collection: School of Medicine
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