Abstract
Non-Alcoholic Steatohepatitis (NASH) is the progressive form of Non-Alcoholic Fatty Liver Disease (NAFLD), the main cause of chronic liver complications. The development of NASH is the consequence of aberrant activation of hepatic conventional immune, parenchymal, and endothelial cells in response to inflammatory mediators from the liver, adipose tissue, and gut. Hepatocytes, Kupffer cells and liver sinusoidal endothelial cells contribute to the significant accumulation of bone-marrow derived-macrophages and neutrophils in the liver, a hallmark of NASH. The aberrant activation of these immune cells elicits harmful inflammation and liver injury, leading to NASH progression. In this review, we highlight the processes triggering the recruitment and/or activation of hepatic innate immune cells, with a focus on macrophages, neutrophils, and innate lymphoid cells as well as the contribution of hepatocytes and endothelial cells in driving liver inflammation/fibrosis. On-going studies and preliminary results from global and specific therapeutic strategies to manage this NASH-related inflammation will also be discussed.
Highlights
Non Alcoholic Fatty Liver Diseases (NAFLDs), recently renamed Metabolic Associated Fatty Liver Diseases (MAFLDs) to better reflect the pathogenesis [1, 2], are the most common chronic liver diseases, with a worldwide prevalence of 25% [3, 4]
NAFLD occurrence appears to be higher in men [10, 11], while postmenopausal women display an increased risk of severe fibrosis compared to men, which can probably be attributed to the loss of the protective effects of estrogen against fibrogenesis [11]
Without underestimating the important role played by the adaptive immune system [reviewed in [34, 35]], the immunological functions of hepatocytes and sentinel cells including liver sinusoidal endothelial cells (LSECs), macrophages, innate lymphoid cells (ILC), and neutrophils according to liver steatosis development and its progression to fibrotic-Non-Alcoholic Steatohepatitis (NASH), which will be debated (Figure 2, Table 1)
Summary
Non Alcoholic Fatty Liver Diseases (NAFLDs), recently renamed Metabolic Associated Fatty Liver Diseases (MAFLDs) to better reflect the pathogenesis [1, 2], are the most common chronic liver diseases, with a worldwide prevalence of 25% [3, 4]. The development of NASH is the consequence of aberrant activation of hepatic conventional immune, parenchymal, and endothelial cells in response to inflammatory mediators from the liver, adipose tissue, and gut.
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