Abstract
Chronic liver disease (CLD) is a growing health concern which accounts for two million deaths per year. Obesity, alcohol overconsumption, and progressive cholestasis are commonly characterized by persistent low-grade inflammation and advancing fibrosis, which form the basis for development of end-stage liver disease complications, including hepatocellular carcinoma. CLD pathophysiology extends to the intestinal tract and is characterized by intestinal dysbiosis, bile acid dysregulation, and gut barrier disruption. In addition, macrophages are key players in CLD progression and intestinal barrier breakdown. Emerging studies are unveiling macrophage heterogeneity and driving factors of their plasticity in health and disease. To date, in-depth investigation of how gut–liver axis disruption impacts the hepatic and intestinal macrophage pool in CLD pathogenesis is scarce. In this review, we give an overview of the role of intestinal and hepatic macrophages in homeostasis and gut–liver axis disruption in progressive stages of CLD.
Highlights
Chronic liver disease (CLD) poses a major global health problem with a mortality rate of approximately two million deaths per year worldwide
The term “CLD” encompasses a group of disorders that are hallmarked by persistent liver inflammation and progressive fibrosis which can progress to hepatocellular carcinoma (HCC) [1,2]
Liver cirrhosis is characterized by intestinal barrier disruption and a disturbed gut–liver crosstalk has been implicated in non-alcoholic fatty liver disease (NAFLD), alcoholic liver disease (ALD), primary sclerosing cholangitis (PSC), liver fibrosis/cirrhosis, and HCC [3,4,5,6,7]
Summary
Chronic liver disease (CLD) poses a major global health problem with a mortality rate of approximately two million deaths per year worldwide. Peripheral infusion of autologous monocyte-derived MFs (MoMFs) was reported to be safe and feasible in cirrhotic patients and may form the basis for new targeted cell-based therapy [10]. In this context, an indepth understanding of the role of MFs in liver diseases, and in gut–liver communication in the context of CLD, is important and may lead to new important insights and more fine-tuned pharmacological approaches. This review focusses on the composition of the intestinal and hepatic MF pool and their subset-specific functions in homeostasis and gut-liver axis disruption, with specific elaboration on NAFLD, ALD, PSC, fibrosis/cirrhosis, and HCC
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