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      Liver Injury and the Macrophage Issue: Molecular and Mechanistic Facts and Their Clinical Relevance

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          Abstract

          The liver is an essential immunological organ due to its gatekeeper position to bypassing antigens from the intestinal blood flow and microbial products from the intestinal commensals. The tissue-resident liver macrophages, termed Kupffer cells, represent key phagocytes that closely interact with local parenchymal, interstitial and other immunological cells in the liver to maintain homeostasis and tolerance against harmless antigens. Upon liver injury, the pool of hepatic macrophages expands dramatically by infiltrating bone marrow-/monocyte-derived macrophages. The interplay of the injured microenvironment and altered macrophage pool skews the subsequent course of liver injuries. It may range from complete recovery to chronic inflammation, fibrosis, cirrhosis and eventually hepatocellular cancer. This review summarizes current knowledge on the classification and role of hepatic macrophages in the healthy and injured liver.

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          Cleavage of GSDMD by inflammatory caspases determines pyroptotic cell death.

          Jianjin Shi, Yue Zhao, Kun Wang … (2015)
          Inflammatory caspases (caspase-1, -4, -5 and -11) are critical for innate defences. Caspase-1 is activated by ligands of various canonical inflammasomes, and caspase-4, -5 and -11 directly recognize bacterial lipopolysaccharide, both of which trigger pyroptosis. Despite the crucial role in immunity and endotoxic shock, the mechanism for pyroptosis induction by inflammatory caspases is unknown. Here we identify gasdermin D (Gsdmd) by genome-wide clustered regularly interspaced palindromic repeat (CRISPR)-Cas9 nuclease screens of caspase-11- and caspase-1-mediated pyroptosis in mouse bone marrow macrophages. GSDMD-deficient cells resisted the induction of pyroptosis by cytosolic lipopolysaccharide and known canonical inflammasome ligands. Interleukin-1β release was also diminished in Gsdmd(-/-) cells, despite intact processing by caspase-1. Caspase-1 and caspase-4/5/11 specifically cleaved the linker between the amino-terminal gasdermin-N and carboxy-terminal gasdermin-C domains in GSDMD, which was required and sufficient for pyroptosis. The cleavage released the intramolecular inhibition on the gasdermin-N domain that showed intrinsic pyroptosis-inducing activity. Other gasdermin family members were not cleaved by inflammatory caspases but shared the autoinhibition; gain-of-function mutations in Gsdma3 that cause alopecia and skin defects disrupted the autoinhibition, allowing its gasdermin-N domain to trigger pyroptosis. These findings offer insight into inflammasome-mediated immunity/diseases and also change our understanding of pyroptosis and programmed necrosis.
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            Global burden of NAFLD and NASH: trends, predictions, risk factors and prevention

            Zobair Younossi, Quentin M Anstee, Milena Marietti … (2018)
            NAFLD is one of the most important causes of liver disease worldwide and will probably emerge as the leading cause of end-stage liver disease in the coming decades, with the disease affecting both adults and children. The epidemiology and demographic characteristics of NAFLD vary worldwide, usually parallel to the prevalence of obesity, but a substantial proportion of patients are lean. The large number of patients with NAFLD with potential for progressive liver disease creates challenges for screening, as the diagnosis of NASH necessitates invasive liver biopsy. Furthermore, individuals with NAFLD have a high frequency of metabolic comorbidities and could place a growing strain on health-care systems from their need for management. While awaiting the development effective therapies, this disease warrants the attention of primary care physicians, specialists and health policy makers.
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              EASL-EASD-EASO Clinical Practice Guidelines for the management of non-alcoholic fatty liver disease.

              Michael Roden (2016)
              Article 0 comments Cited 1284 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Rolf Teschke: Role: Academic Editor
                Leo A. van Grunsven: Role: Academic Editor
                Journal
                Journal ID (nlm-ta): Int J Mol Sci
                Journal ID (iso-abbrev): Int J Mol Sci
                Journal ID (publisher-id): ijms
                Title: International Journal of Molecular Sciences
                Publisher: MDPI
                ISSN (Electronic): 1422-0067
                Publication date (Electronic): 06 July 2021
                Publication date Collection: July 2021
                Volume: 22
                Issue: 14
                Electronic Location Identifier: 7249
                Affiliations
                Department of Hepatology and Gastroenterology, Campus Virchow-Klinikum and Campus Charité Mitte, Charité University Medicine Berlin, 13353 Berlin, Germany; Siyer.Roohani@ 123456charite.de
                Author notes
                Author information
                https://orcid.org/0000-0001-6206-0226
                Article
                Publisher ID: ijms-22-07249
                DOI: 10.3390/ijms22147249
                PMC ID: 8306699
                PubMed ID: 34298870
                SO-VID: 3dd994fa-e08b-454c-98c7-fceda154cc4c
                Copyright © © 2021 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( https://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 15 June 2021
                Date accepted : 01 July 2021
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular biology
                Keywords: hepatic macrophages,kupffer cells,monocyte-derived macrophages,acute liver injury,chronic liver injury,nafld,nash,liver fibrosis,hbv,hcv
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: hepatic macrophages, kupffer cells, monocyte-derived macrophages, acute liver injury, chronic liver injury, nafld, nash, liver fibrosis, hbv, hcv

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