Abstract
Liver sinusoidal endothelial cells (LSECs) play a pivotal role in hepatic function and homeostasis. LSEC dysfunction has been recognized to be closely involved in various liver diseases, including non-alcoholic steatohepatitis (NASH), but not much is known about the fate of the scavenger receptors in LSECs during NASH. Fc gamma receptor IIb (FcγRIIb), known as a scavenger receptor, contributes to receptor-mediated endocytosis and immune complexes clearance. In this study, to elucidate the fate of FcγRIIb in the progression of non-alcoholic fatty liver disease (NAFLD), we examined FcγRIIb levels in NAFLD biopsy specimens by immunohistochemistry, and investigated their correlation with the exacerbation of biological indexes and clinicopathological scores of NASH. The FcγRIIb expression levels indicated significant negative correlations with serum levels of blood lipids (triglyceride, total cholesterol, high-density lipoprotein-cholesterol), type 4 collagen and hyaluronic acid, which are involved in hepatic lipid metabolism disorder, fibrosis, and inflammation, respectively. However, there was no significant difference of FcγRIIb expression levels among the pathological grades of NAFLD. During NAFLD progression, inflammation and fibrosis may influence the expression of FcγRIIb and their scavenger functions to maintain hepatic homeostasis.
Highlights
Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic syndrome and is categorized into non-alcoholic fatty liver (NAFL), with simple fatty liver, and non-alcoholic steatohepatitis (NASH), with inflammation and fibrosis
With the biopsy-proven pathological examination, two patients were diagnosed as NAFL and 24 patients as NASH
The two patients diagnosed with NAFL are listed from the top, followed by the 24 diagnosed as NASH, in ascending order of NAFLD activity score (NAS) and ascending ALT value. This suggests that the serum ALT level is not a sufficient indicator of NASH progression, though it is used as one of the screening criterions for NAFLD
Summary
Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic syndrome and is categorized into non-alcoholic fatty liver (NAFL), with simple fatty liver, and non-alcoholic steatohepatitis (NASH), with inflammation and fibrosis. NAFL is a benign disease, but NASH can lead to severe chronic hepatic diseases, such as advanced fibrosis [1], cirrhosis [2], and hepatocellular carcinoma (HCC) [3, 4]. A multiple parallel-hit hypothesis [6] has been attracting a lot of attention. The multiple factors (e.g., inflammation from gut-derived endotoxin or adipocytokines, endoplasmic reticulum stress, and innate immunity) may act in parallel and lead to the progression of steatosis, hepatocellular ballooning, inflammation, and fibrosis.
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