RNA-Seq and proteomics of Crohn's disease: Terminal ileum of inflamed and non inflamed paired tissue biopsy

The cause of chronic inflammation manifestations such as inflammatory
bowel disease (IBD) is still not yet fully understood. Evidence however
points to the convergence of environmental factors, genetic factors,
intestinal microbiota and the immune response at the intestinal epithelial
surface that consequently leads to a breakdown of barrier function in IBD.
An increasing number of theories implicate a dysfunctional intestinal
epithelial surface in the pathogenesis of IBD and progression to
complicated disease, which contributes significantly to the IBD burden. As
yet, the significance of the intestinal epithelial surface in IBD
manifestation and progression has not been explored using a systems
biology approach, that compares the mucosa of healthy patients to those
with IBD. In the context of dyregulation of the epithelial barrier, there
is a scarcity of publications that explore the contribution of proteins-
the effectors of the cells and RNA message in the pathways affected by CD
and in particular the localization of inflammatory response. We aim to
evaluate the functional pathways of chronic inflammation at the intestinal
epithelial surface using a combination of transcriptomic and proteomic
analyses on intestinal epithelial tissue samples from paired inflamed and
non-inflammed Crohn’s disease (CD) and healthy control subjects.
Concordance of several biological pathways from both data sets was found
to be altered in CD patients’ epithelia when compared to healthy controls.
This information could be helpful in identifying novel therapeutic targets
that aim to restore barrier function at the intestinal epithelial surface
and to guide therapy.