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Updated: May 20, 2025

Investigating Intestinal Inflammation in DSS-induced Model of IBD
Published on: February 1, 2012
Inflammatory Bowel Disease from the Perspective of Newer Innate Immune System Biomarkers
Martin Tobi1, Fadi Antaki1, MaryAnn Rambus1
1Department of Research and Development, Detroit John D. Dingle VAMC, Detroit, MI 48201, USA.
Background:
The perspective of inflammatory bowel disease (IBD) has changed radically since the first decade of the 21st century, and the formerly monolithic components of IBD, ulcerative colitis (UC), and Crohn's disease (CD) have undergone a fundamental convergence, with realization that there is likely an element of shared pathogenesis. The ground shift began with genomic revelation but with the current emergence of the innate immune system (InImS) as a key player, allowing for improved understanding of the associations between the immune underpinnings of IBD.
Methods:
Using unique ferritin/fecal p87 (FERAD) or using colonoscopic effluent as denominator (FEREFF) and other ratios to test this hypothesis, we prospectively enrolled 2185 patients with increased risk of colorectal cancer, of whom 31 had UC and 18 CD, with 2136 controls and brought to bear in a convenient measure for the InImS, the FERAD ratio. The FERAD, FEREFF, and NLR ratios have been shown to be effective measures of the InImS in COVID-19 and various cancers. p87 is expressed in gut Paneth cells known to modulate the microbiome by secretion of alpha-defensins, a natural antibiotic. Other related parameters were also evaluated.
Results:
There was no significant difference between the FERAD ratio in UC and CD. However, differences between IBD entities and controls were substantial.
Conclusions:
InImS settings in IBD are similar between CD and UC. p87 tissue immunohistochemistry (IHC) is also shared. Other InImS markers, such as the absolute neutrophil/lymphocyte ratio, are also confluent between the two IBD forms.
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