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Review
. 2019 Jun;32(1):128-145.
doi: 10.1017/S0954422418000239. Epub 2019 Feb 1.

Interplay between early-life malnutrition, epigenetic modulation of the immune function and liver diseases

Sabrina Campisano  1 , Anabela La Colla  1 , Stella M Echarte  1 , Andrea N Chisari  1
Affiliations
Review

Interplay between early-life malnutrition, epigenetic modulation of the immune function and liver diseases

Sabrina Campisano et al. Nutr Res Rev. 2019 Jun.

Abstract

Early-life nutrition plays a critical role in fetal growth and development. Food intake absence and excess are the two main types of energy malnutrition that predispose to the appearance of diseases in adulthood, according to the hypothesis of 'developmental origins of health and disease'. Epidemiological data have shown an association between early-life malnutrition and the metabolic syndrome in later life. Evidence has also demonstrated that nutrition during this period of life can affect the development of the immune system through epigenetic mechanisms. Thus, epigenetics has an essential role in the complex interplay between environmental factors and genetics. Altogether, this leads to the inflammatory response that is commonly seen in non-alcoholic fatty liver disease (NAFLD), the hepatic manifestation of the metabolic syndrome. In conjunction, DNA methylation, covalent modification of histones and the expression of non-coding RNA are the epigenetic phenomena that affect inflammatory processes in the context of NAFLD. Here, we highlight current understanding of the mechanisms underlying developmental programming of NAFLD linked to epigenetic modulation of the immune system and environmental factors, such as malnutrition.

Keywords: ATF-like-3; BAFF B cell activating factor; Batf3 basic leucine zipper transcription factor; CCL C-C motif chemokine ligand; CXCL chemokine (C-X-C motif) ligand; DC dendritic cells; DNMT DNA methyltransferases; HCC hepatocellular carcinoma; HDAC histone deacetylase; HFD high-fat diet; HSC hepatic stellate cells; KC Kupffer cells; MDSC myeloid-derived suppressor cells; MT-ND6 mitochondrial NADH dehydrogenase 6; NAFLD non-alcoholic fatty liver disease; NASH non-alcoholic steatohepatitis; NK natural killer; NKT natural killer T; NLR NOD-like receptor; SAM S-adenosylmethionine; SEC sinusoidal endothelial cells; SIRT sirtuin; SOCS suppressor of cytokine signalling; T2DM type 2 diabetes mellitus; TGF-β transforming growth factor-β; TLR Toll-like receptor; lncRNA long non-coding RNA; mDC myeloid dendritic cells; miRNA microRNA; pDC plasmacytoid dendritic cells; Early malnutrition; Epigenetics; Immune response; Liver disease.

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