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.

Residual Effects of Restless Sleep over Depressive Symptoms on Chronic Medical Conditions: Race by Gender Differences

“…Significant evidence has shown dysregulation of homeostatic buffering mechanisms regulating oxidation and inflammation that exist in healthy individuals in the presence of depression, sleep disorder, and CMC (95). Thus, changes in inflammation, oxidative stress and immune function may be the mechanisms that at least in part explain the effect of depression and poor sleep on CMC over time (96–100). It is still not clear if peripheral and central inflammation fully mediate the comorbidities between poor sleep, depression, and CMC (101).…”

Genome‐Wide Transcriptional Analysis Reveals the Protection against Hypoxia‐Induced Oxidative Injury in the Intestine of Tibetans via the Inhibition of GRB2/EGFR/PTPN11 Pathways

“…All the changes can be caused by oxidative stress, such as cancer suppressor [23], cell normal functions [24], special responses for pathogens [25], maximal actions, and antigen presentation [26] (Figure 6). Pathway analysis revealed that, in intestinal mucosa tissues of participants from high altitude, many pathway genes had aberrant expression and may be also related with oxidative stress, especially in inflammatory bowel diseases [27, 28], myeloperoxidase [29], ROS production [10], apoptotic cell death [30], tissue damage [31], interleukin-1 [32], oxidative modification [33], cystic fibrosis [34], natural killer cells activity [35], lymphocytes [36], fibrinolysis [37] and so on (Figure 7). …”

The Perception of Physician Empathy by Patients with Inflammatory Bowel Disease

“…Interestingly, a recent study reported that depression has a similar pathophysiology to that of IBD, i.e. they are both clinical expressions of activated immune-inflammatory, oxidative, and nitric oxid stress pathways, which may explain the frequent co-occurrence of these two conditions [23]. Another recent study found a strong relationship between perceived stress and gastrointestinal symptoms [24].…”