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A gene expression map of colon tissue in ulcerative colitis: new methods rewrite old stories

© Biotarget. All rights reserved. Biotarget 2020 | http://dx.doi.org/10.21037/biotarget.2020.01.02 Ulcerative colitis (UC) constitutes a chronic relapsing inflammatory disease of the colonic mucosa with increasing incidence in all ages that imparts significant morbidity; As therapeutic options remain limited, UC urges as an important health concern worldwide (1,2). Along with Crohn’s disease (CD) represent the two main types of inflammatory bowel disease (IBD). Besides their phenotypic similarities there are substantial differences between UC and CD. Inflammation pattern in UC is uninterrupted and is restricted to colonic mucosa, while in CD is patchy and may affect any part of the gastrointestinal tract in a transmural fashion often leading to fibrotic complications. These differences probably reflect the distinctive cellular mechanisms and pathways underlining their respective pathogenesis (3,4). Despite extensive investigations over the last years the pathogenesis of UC remains incompletely understood. It is suggested that complex interactions among genetic, immune, microbial and environmental factors disrupt the homeostatic mechanisms in colonic mucosa leading to disease development. Today, there is a pressing need for a better understanding of UC pathogenesis that will provide novel molecular mechanisms and targets permitting tailored therapeutic approaches to individual patients with UC (1,3,4). To this end, several different approaches have been used in order to nominate candidate molecular pathways in the pathogenesis of inflammation in UC and reveal biomarkers that can predict disease relapse or response to treatment. In hypothesis-driven studies, several candidate genes, proteins, and/or cell populations have been analyzed at intestinal tissue level or in peripheral blood in an attempt to correlate UC clinical traits with certain molecular characteristics. Over the last years, these approaches have proposed a variety of molecular mechanisms offering potential models responsible for gut inflammation in UC (3,4); however they did not fully elucidate the pathophysiology of this complex disease. It seems puzzling over how to assess different cell populations and molecules that dynamically interplay in the continuously altered microenvironment of inflamed intestinal mucosa of UC. On the other hand, in the new “omics era”, highthroughput, discovery-driven approaches such as genomics, transcriptomics, proteomics and metabolomics have emerged providing a deeper and more comprehensive analysis of molecular biology of UC (5-8). Numerous bioinformatics-based tools have been developed to explore and integrate the huge amount of data generated by multi“omics” profiling, aiming at characterizing the molecular “UC interactome” (Figure 1). Recently, Smillie et al. (9), used a novel approach by applying single-cell RNA sequencing (scRNA-seq) analysis Editorial Commentary