Colonic Mucosal Interleukin 1 Receptor Antagonist in Inflammatory Bowel Disease

Digestion ◽  
1994 ◽  
Vol 55 (6) ◽  
pp. 368-373 ◽  
Author(s):  
Tsutomu Nishiyama ◽  
Keiichi Mitsuyama ◽  
Atsushi Toyonaga ◽  
Ei Sasaki ◽  
Kyuichi Tanikawa
1994 ◽  
Vol 39 (9) ◽  
pp. 1893-1899 ◽  
Author(s):  
Jeffrey S. Hyams ◽  
John E. Fitzgerald ◽  
Nancy Wyzga ◽  
William R. Treem ◽  
Christopher J. Justinich ◽  
...  

2002 ◽  
Vol 3 (7) ◽  
pp. 400-406 ◽  
Author(s):  
L Vijgen ◽  
M Van Gysel ◽  
A Rector ◽  
I Thoelen ◽  
N Esters ◽  
...  

2012 ◽  
Vol 194 (1) ◽  
pp. 66-70 ◽  
Author(s):  
Shingo Maeda ◽  
Koichi Ohno ◽  
Kenji Nakamura ◽  
Kazuyuki Uchida ◽  
Ko Nakashima ◽  
...  

CNS Spectrums ◽  
2015 ◽  
Vol 21 (2) ◽  
pp. 184-198 ◽  
Author(s):  
Marta Martin-Subero ◽  
George Anderson ◽  
Buranee Kanchanatawan ◽  
Michael Berk ◽  
Michael Maes

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.


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