Epigenetic Changes in Chronic Inflammatory Diseases

被引：43
作者：
Fogel, O. [1 ,2 ]
Richard-Miceli, C. [1 ,3 ]
Tost, J. [2 ]
机构：
[1] Univ Paris 05, Hop Cochin, Assistance Publ Hop Paris, EULAR Ctr Excellence, Paris, France
[2] CEA, Inst Genom, Ctr Natl Genotypage, Lab Epigenet & Environm, Evry, France
[3] Inst Pasteur, Immunoregulat Unit, Unite Mixte Pasteur, APHP, Paris, France
来源：
CHROMATIN REMODELLING AND IMMUNITY | 2017年 / 106卷
关键词：
WIDE DNA METHYLATION; HISTONE DEACETYLASE INHIBITORS; ULCERATIVE-COLITIS; CROHNS-DISEASE; BOWEL-DISEASE; CPG SITES; T-CELLS; MACROPHAGE POLARIZATION; ANKYLOSING-SPONDYLITIS; PROMOTER METHYLATION;
D O I：
10.1016/bs.apcsb.2016.09.003
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
The number of people diagnosed with chronic inflammatory diseases has increased noteworthy in the last 40 years. Spondyloarthritis (SpA), inflammatory bowel diseases (IBD), and psoriasis are the most frequent chronic inflammatory diseases, resulting from a combination of genetic predisposition and environmental factors. Epigenetic modifications include DNA methylation, histone modifications, and small and long non-coding RNAs. They are influenced by environmental exposure, life-style, and aging and have recently been shown to be altered in many complex diseases including inflammatory diseases. While epigenetic modifications have been well characterized in other diseases such as cancer and autoimmune diseases, knowledge on changes in inflammatory diseases is lagging behind with some disease-specific differences. While the DNA methylation profile of different cell types in patients with IBD has been relatively well described, less is known on changes implicated in psoriasis, and no systematic genome-wide studies have so far been performed in SpA. In this chapter, we review in detail the reported changes in patterns of DNA methylation and posttranslational histone modifications in chronic inflammatory diseases highlighting potential connections between disease-associated pathophysiological changes such as the dysbiosis of the microbiome or genetic variations associated with disease susceptibility and the epigenome. We also discuss important parameters of meaningful epigenetic studies such as the use of well defined, disease-relevant cell populations, and elude on the potential future of engineering of the epigenome in inflammatory diseases.
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页码：139 / 189
页数：51
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