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• W3161931973 abstract "Aims: The pathophysiology of non-alcoholic steatohepatitis (NASH) is multifactorial and not yet completely understood; however, innate immunity is a major contributing factor in which liver-resident macrophages (Kupffer cells) and recruited macrophages play a central part in disease progression. In this study, we aimed to demonstrate that activated macrophages are as key mediators of inflammation and fibrosis progression in NASH livers.Methods: Ninety-four, snap-frozen benign liver tissues with various chronic liver diseases in the different fibrosis stages (0: n=17, 1: n=12, 2: n=12, 3: n=25, 4: n=28) were subjected to the expression analyses. Gene expression analysis was performed using the nCounter PanCancer Pathway Panel (NanoString Technologies, Seattle, WA, USA). Liver biopsy was performed for NASH livers with various fibrosis stages. Immunohistochemistry and multicolor flow cytometry were performed with the biopsy specimen. Mouse model of NASH-induced liver cirrhosis was established using high-fat, high-cholesterol (HFHC) diet with intraperitoneal streptozocin injection. All statistical analyses in this study were performed using the open source statistical programming environment R language (version 3.4.3).Results: Gene expression analysis with 94 patient liver samples using the nCounter PanCancer Pathway Panel identified that expression level of IL12B, SOCS1, and STAT1, which are robustly expressed in activated macrophages, was higher in the livers with advanced fibrosis (stage 3 and 4) than those with low-grade fibrosis (stage 1 and 2) or no fibrosis (P<0.001). Immunohistochemical staining demonstrated that the number of CD68+ macrophages increases as the fibrosis progresses in NASH livers (P<0.05). Flow cytometry using liver biopsy specimen demonstrated that macrophages in the livers with advanced fibrosis show higher expression of HLA-DR and PDL1, suggesting that these macrophages contribute not only to the inflammation and fibrosis, but also to dismantling anti-tumor immune surveillance in fibrotic NASH livers. Mice fed with HFHC diet with intraperitoneal streptozocin injection developed NASH, liver cirrhosis, and hepatocellular carcinoma, and the number of activated macrophages increased as the disease progressed.Conclusions: Our data using expression analysis of immune markers showed that activated macrophages are key mediators of inflammation and fibrosis progression in NASH livers. This study was supported by The Research Supporting Program of The Korean Association for the Study of the Liver and The Korean Liver Foundation. This study was also supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIT) (2020R1A2C3011569)." @default.
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• W3161931973 date "2020-01-01" @default.
• W3161931973 modified "2023-10-16" @default.
• W3161931973 title "PE-202 : Expression Analysis of Immune Markers in Non-Alcoholic Steatohepatitis Identifies Activated Macrophages as Key Mediators of Inflammation and Fibrosis Progression" @default.
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