Expression of CD68 and Fas Ligand in Colon Mucosa of Patients with Inflammatory Bowel Disease as Prognostic Markers of Cancerogenesis

2016 ◽  
Vol 7 (3) ◽  
pp. 42-48
Author(s):  
Andrey V Santimov ◽  
Andrey V Kolobov ◽  
Vadim E Karev ◽  
Oksana L Kolobova ◽  
Mikhail M Kostik ◽  
...  

As it is known, colon carcinogenesis is associated with the inflammatory bowel disease (IBD). Colorectal cancer (CRC) being observed in 5.5-13.5 % of patients with ulcerative colitis (UC) and in 0.4-0.8 % of patients with Crohn disease (CD). The gut mucosa of patients with CD, but not with UC, as well as the stroma of CRC have elevated numbers of CD68(+) macrophages. It is known also that the expression of Fas Ligand (FasL), representing another branch of immunoreactivity, in the lesions of CRC and UC but not of CD is upregulated. The fact that enterocyte apoptosis is increased in lesions of CD and lymphocytes in UC are resistant to Fas-mediated apoptosis can be the keypoint for understanding the hypothesis [17], suggesting that cells express FasL and are able to kill Fas-expressing activated lymphocytes and escape rejection by the immune system, which can be the basis for differences in association of UC and CD with CRC. The aim of this study was to evaluate the number of CD68(+) macrophages and to analyze FasL expression in colon mucosa of patients with UC, CD and CRC in order to assess its value for prognosis of CRC. Expression of CD68 and FasL was analyzed immunohistochemically in the samples of colon mucosa taken from the affected areas of 4 patients with UC, 6 patients with CD and 10 patients with CRC. In addition in 7 CRC patients the samples taken from unaffected areas were analyzed. We find average expression of FasL in both unaffected and affected areas of CRC patients was higher than in CD patients (p = 0.04, p = 0.00). Average expression of FasL in affected areas of CRC patients was higher (p = 0.02) than in UC patients and the same (p = 0.23) as in unaffected areas of CRC patients. The revealed associations support the possibility to use expression of CD68 and FasL as prognostic markers for transformation of IBD to CRC.

2018 ◽  
Vol 1 (1) ◽  
pp. 15-29 ◽  
Author(s):  
Ranmali Ranasinghe ◽  
Rajaraman Eri

Inflammatory bowel disease (IBD) has evoked significant interest in human immunobiology given its tactical immune evasion methodologies resulting in acute immune destabilization. IBD comprising Crohn’s disease and Ulcerative colitis manifests as chronic inflammation in the gut mucosa, leading to complexities involving immune dysregulation in the T helper lymphocyte arm, effecting disease pathogenicity. The mucosa of the alimentary canal is constantly exposed to a myriad of food antigens and luminal microorganisms for which a consistent host-protective mechanism is operative in healthy people. Lowered mucosal immune expression which allows penetration of the epithelial barrier by infective pathogenic microbes elicits both innate and adaptive immune responses in the gut, culminating in aberrant intestinal inflammation. Interestingly, the IBD leukocyte repertoire is significantly entwined with chemokine-assisted chemotactic navigation into the sites of inflammation, which is also thought to generate favorable immune-suppressive responses. The functions of the cognate chemokine receptor, CCR6, which binds with its unique ligand CCL20, are expected to tilt the balance between upregulation of homeostatic tolerance and inflammatory pathophysiology. This review aims to critically examine the CCR6-driven immune pathways: TH1/TH2, TH1/TH17, TH17/Treg, IL-23/IL-17, Akt/ERK-1/2, ILC3, and TH9/TH2 for systematic investigation of its underlying mechanisms in the future and to underpin its importance in resolving IBD pathology. Thus, CCR6 occupies an exclusive position in gut immunology which renders it an invaluable therapeutic tool for the production of novel medicaments to treat IBD.


Gut ◽  
1989 ◽  
Vol 30 (2) ◽  
pp. 188-194 ◽  
Author(s):  
E de Jong ◽  
R J Porte ◽  
E A Knot ◽  
J H Verheijen ◽  
J Dees

Gut ◽  
1996 ◽  
Vol 38 (2) ◽  
pp. 216-222 ◽  
Author(s):  
R Daig ◽  
T Andus ◽  
E Aschenbrenner ◽  
W Falk ◽  
J Scholmerich ◽  
...  

1995 ◽  
Vol 1 (2) ◽  
pp. 142-158 ◽  
Author(s):  
Steven H. Itzkowitz ◽  
Bruce Greenwald ◽  
Stephen J. Meltzer

2015 ◽  
Vol 82 (4) ◽  
pp. 352-360 ◽  
Author(s):  
T. J. Ślebioda ◽  
A. Bojarska-Junak ◽  
M. Stanisławowski ◽  
M. Cyman ◽  
P. M. Wierzbicki ◽  
...  

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