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. 2020 Jan 30;43(3):1054–1064. doi: 10.1007/s10753-020-01190-4

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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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — The role of IL-1β activation pathways in NAFLD. Pro-inflammatory cytokines contribute to NAFLD development from liver steatosis to NASH and fibrosis by activating sterile inflammation in the liver. Some of these cytokines such as IL-1β and IL-18 are secreted as inactive and need proteolytic cleavage in order to become active. Two mechanisms responsible for IL-1 cytokine activation are represented by the NLRP3 inflammasome-caspase-1 protein complex and the neutrophil serine proteases PR3 and NE. Additionally to IL-1β and IL-18, PR3 and NE are able to activate membrane-bound TNF. Activating pro-inflammatory NLRP3 inflammasome-caspase-1 complex and the neutrophil serine proteases also contributes to NAFLD development and progression. IL-1β, interleukin-1β; IL-18, interleukin-18; NASH, non-alcoholic steatohepatitis; NE, neutrophil elastase; PR3, proteinase-3; Pro-IL-1β, pro-interleukin-1β; Pro-IL-18, pro-interleukin-18; TNF, tumor necrosis factor.