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Inflammatory bowel disease - one entity with many molecular faces.

ABSTRACT: Inflammatory bowel disease (IBD) is a heterogenous group of chronic inflammations in the gastrointestinal tract, which traditionally consists of two types: Crohn's disease and ulcerative colitis. They differ when it comes to clinical, endoscopic, and histopathological changes. The exact aetiology of IBD has not been fully comprehended, but what is known so far is that the aetiopathogenesis of the disease is compound. Many articles have been written on the cellular/molecular background of IBD. Based on various molecular pathways, new forms of the disease have been discovered, including very early-onset IBD (VEO-IBD) or IBD coexisting with primary sclerosing cholangitis. The aim of this article is to present the molecular mechanisms leading to IBD, focusing on new forms of this disorder.

SUBMITTER: Szymanska S

PROVIDER: S-EPMC6983764 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Inflammatory bowel disease - one entity with many molecular faces.

Szymańska Sylwia S Matuszczyk Malgorzata M Osuch Magdalena M Meglicka Monika M Szymanska Edyta E Bierła Joanna J Kierkuś Jaroslaw J

Przeglad gastroenterologiczny 20191220 4

Inflammatory bowel disease (IBD) is a heterogenous group of chronic inflammations in the gastrointestinal tract, which traditionally consists of two types: Crohn's disease and ulcerative colitis. They differ when it comes to clinical, endoscopic, and histopathological changes. The exact aetiology of IBD has not been fully comprehended, but what is known so far is that the aetiopathogenesis of the disease is compound. Many articles have been written on the cellular/molecular background of IBD. Ba ...[more]

PMID: 31988668

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Project description:Natural and synthetic glucocorticoids (GCs) are widely employed in a number of inflammatory, autoimmune and neoplastic diseases, and, despite the introduction of novel therapies, remain the first-line treatment for inducing remission in moderate to severe active Crohn's disease and ulcerative colitis. Despite their extensive therapeutic use and the proven effectiveness, considerable clinical evidence of wide inter-individual differences in GC efficacy among patients has been reported, in particular when these agents are used in inflammatory diseases. In recent years, a detailed knowledge of the GC mechanism of action and of the genetic variants affecting GC activity at the molecular level has arisen from several studies. GCs interact with their cytoplasmic receptor, and are able to repress inflammatory gene expression through several distinct mechanisms. The glucocorticoid receptor (GR) is therefore crucial for the effects of these agents: mutations in the GR gene (NR3C1, nuclear receptor subfamily 3, group C, member 1) are the primary cause of a rare, inherited form of GC resistance; in addition, several polymorphisms of this gene have been described and associated with GC response and toxicity. However, the GR is not self-standing in the cell and the receptor-mediated functions are the result of a complex interplay of GR and many other cellular partners. The latter comprise several chaperonins of the large cooperative hetero-oligomeric complex that binds the hormone-free GR in the cytosol, and several factors involved in the transcriptional machinery and chromatin remodeling, that are critical for the hormonal control of target genes transcription in the nucleus. Furthermore, variants in the principal effectors of GCs (e.g. cytokines and their regulators) have also to be taken into account for a comprehensive evaluation of the variability in GC response. Polymorphisms in genes involved in the transport and/or metabolism of these hormones have also been suggested as other possible candidates of interest that could play a role in the observed inter-individual differences in efficacy and toxicity. The best-characterized example is the drug efflux pump P-glycoprotein, a membrane transporter that extrudes GCs from cells, thereby lowering their intracellular concentration. This protein is encoded by the ABCB1/MDR1 gene; this gene presents different known polymorphic sites that can influence its expression and function. This editorial reviews the current knowledge on this topic and underlines the role of genetics in predicting GC clinical response. The ambitious goal of pharmacogenomic studies is to adapt therapies to a patient's specific genetic background, thus improving on efficacy and safety rates.

Dataset Information

Inflammatory bowel disease - one entity with many molecular faces.

Publications

Inflammatory bowel disease - one entity with many molecular faces.

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