Abstract
Obesity is a prevalent predisposing factor to non-alcoholic fatty liver disease (NAFLD), the most common chronic liver disease in the developed world. NAFLD spectrum of disease involves progression from steatosis (NAFL), to steatohepatitis (NASH), cirrhosis and hepatocellular carcinoma (HCC). Despite clinical and public health significance, current FDA approved therapies for NAFLD are lacking in part due to insufficient understanding of pathogenic mechanisms driving disease progression. The etiology of NAFLD is multifactorial. The induction of both systemic and tissue inflammation consequential of skewed immune cell metabolic state, polarization, tissue recruitment, and activation are central to NAFLD progression. Here, we review the current understanding of the above stated cellular and molecular processes that govern macrophage contribution to NAFLD pathogenesis and how adipose tissue and liver crosstalk modulates macrophage function. Notably, the manipulation of such events may lead to the development of new therapies for NAFLD.
Highlights
The unabated obesity pandemic is directly linked with the incidence of non-alcoholic fatty liver disease (NAFLD)
NAFLD spectrum of disease progresses from non-alcoholic fatty liver (NAFL) or hepatic steatosis, to non-alcoholic steatohepatitis (NASH), to cirrhosis and hepatocellular carcinoma (HCC)
The contribution of various immune cells in hepatic inflammation and the mechanisms that govern their migration to the liver, polarization, and inflammatory capabilities, in NAFLD progression represent an intense area of investigation
Summary
The unabated obesity pandemic is directly linked with the incidence of non-alcoholic fatty liver disease (NAFLD). The contribution of various immune cells in hepatic inflammation and the mechanisms that govern their migration to the liver, polarization, and inflammatory capabilities, in NAFLD progression represent an intense area of investigation. Both liver resident (e.g., Kupffer cells, [KC], hepatic stellate cells, [HSC], hepatocytes) and infiltrating immune cells (e.g., neutrophils, dendritic cells [DC], natural killer [NK] cells, NKT cells, blood monocytes, T cells, B cells, and macrophages) contribute to NAFLD development and progression via systemic and tissue inflammatory mediator production (e.g., interleukin [IL]-17A, IL-6, tumor necrosis factor [TNF], IL-1β) [5, 11].
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