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. 2020 May 26;52(5):772–780. doi: 10.1038/s12276-020-0438-5

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Alcohol consumption induces lipolysis in adipocytes and inflammatory responses in adipose immune cells, including macrophages, which in turn lead to the release of free fatty acids (FFAs), adipokines (e.g., leptin), and cytokines (e.g., TNF-α and IL-6) into the portal circulation. In addition, alcohol intake alters the gut microbiome composition and increases the permeability of intestinal bacteria and their metabolites through broken barriers of epithelial cells in the gut, thus leading to translocation of bacteria and inflammatory cells in the liver. Therefore, metabolic and immunogenic factors, including DAMPs and PAMPs, from adipose tissue and the gut enter the liver, affecting hepatocytes and non-parenchymal cells in the liver to recruit pro-inflammatory immune cells from the bone marrow. Taken together, inter-organ cross-talk between the liver and other organs plays a critical role in the pathogenesis of ALD.