Abstract
Inflammatory bowel disease (IBD) is a chronic relapsing/remitting inflammatory illness of the gastrointestinal tract of unknown aetiology. Despite recent advances in decoding the pathophysiology of IBD, many questions regarding disease pathogenesis remain. Genome-wide association studies (GWAS) and knockout mouse models have significantly advanced our understanding of genetic susceptibility loci and inflammatory pathways involved in IBD pathogenesis. Despite their important contribution to a better delineation of the disease process in IBD, these genetic findings have had little clinical impact to date. This is because the presence of a given gene mutation does not automatically correspond to changes in its expression or final metabolic or structural effect(s). Furthermore, the existence of these gene susceptibility loci in the normal population suggests other driving prerequisites for the disease manifestation. Proteins can be considered the main functional units as almost all intracellular physiological functions as well as intercellular interactions are dependent on them. Proteomics provides methods for the large-scale study of the proteins encoded by the genome of an organism or a cell, to directly investigate the proteins and pathways involved. Understanding the proteome composition and alterations yields insights into IBD pathogenesis as well as identifying potential biomarkers of disease activity, mucosal healing, and cancer progression. This review describes the state of the art in the field with respect to the study of IBD and the potential for translation from biomarker discovery to clinical application.
Highlights
Inflammatory bowel disease (IBD) is an idiopathic chronic condition of unknown aetiology with an inflammatory gut response to unidentified triggers
Two-dimensional poly-acrylamide gel electrophoresis (2DE) and liquid chromatography (LC) are amongst the common tools used in separation of a large amount of proteins followed by mass spectrometry- (MS-) based techniques for relative quantification of proteins
We proposed a model for the pathogenesis of colitis-associated colorectal cancer (CAC) whereby acute inflammation reduces keratin levels and affects mucosal Intermediate filaments (IF) protein integrity which lags behind apparent clinical, microscopic, and endoscopic recovery; persistent failure of such recovery may be the cornerstone of pathogenesis of CAC [172]
Summary
IBD is an idiopathic chronic condition of unknown aetiology with an inflammatory gut response to unidentified triggers. It broadly encompasses two major disease categories, namely, ulcerative colitis and Crohn’s disease, with a relapsing and remitting course. Crohn’s disease (CD) is characterised by discontinuous areas of transmural inflammation It can involve any part of the gastrointestinal tract, the terminal ileum and proximal colon are more frequently affected. The role of innate mucosal immunity such as epithelial barrier integrity, microbial sensing, autophagy, and unfolded protein response is becoming more evident in regulating an appropriate inflammatory response in IBD [28, 29]. Proteomics enables biomarker discovery by providing methods for identification and quantification of proteins and comparative profiling of complex biological samples
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