Comorbidity between depression and inflammatory bowel disease explained by immune-inflammatory, oxidative, and nitrosative stress; tryptophan catabolite; and gut–brain pathways
Data(s) |
01/04/2016
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Resumo |
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. |
Identificador | |
Idioma(s) |
eng |
Publicador |
Cambridge University Press |
Relação |
http://dro.deakin.edu.au/eserv/DU:30078426/berk-comorbiditybetween-inpress-2015.pdf http://dro.deakin.edu.au/eserv/DU:30078426/martin-subero-comorbiditybetween-2016.pdf http://www.dx.doi.org/10.1017/S1092852915000449 |
Direitos |
2016 Cambridge University Press |
Palavras-Chave | #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 |
Tipo |
Journal Article |