Dietary factors alter hepatic innate immune system in mice with nonalcoholic fatty liver disease

Hepatology ◽  
2005 ◽  
Vol 42 (4) ◽  
pp. 880-885 ◽  
Author(s):  
Zhiping Li ◽  
Mark J. Soloski ◽  
Anna Mae Diehl
2021 ◽  
pp. 1-11
Author(s):  
Marina Nati ◽  
Kyoung-Jin Chung ◽  
Triantafyllos Chavakis

Nonalcoholic fatty liver disease (NAFLD) is a very common hepatic pathology featuring steatosis and is linked to obesity and related conditions, such as the metabolic syndrome. When hepatic steatosis is accompanied by inflammation, the disorder is defined as nonalcoholic steatohepatitis (NASH), which in turn can progress toward fibrosis development that can ultimately result in cirrhosis. Cells of innate immunity, such as neutrophils or macrophages, are central regulators of NASH-related inflammation. Recent studies utilizing new experimental technologies, such as single-cell RNA sequencing, have revealed substantial heterogeneity within the macrophage populations of the liver, suggesting distinct functions of liver-resident Kupffer cells and recruited monocyte-derived macrophages with regards to regulation of liver inflammation and progression of NASH pathogenesis. Herein, we discuss recent developments concerning the function of innate immune cell subsets in NAFLD and NASH.


Author(s):  
Jingjing Cai ◽  
Meng Xu ◽  
Xiaojing Zhang ◽  
Hongliang Li

The physiological significance of innate immune signaling lies primarily in its role in host defense against invading pathogens. It is becoming increasingly clear that innate immune signaling also modulates the development of metabolic diseases, especially nonalcoholic fatty liver disease and cardiovascular diseases, which are characterized by chronic, low-grade inflammation due to a disarrangement of innate immune signaling. Notably, recent studies indicate that in addition to regulating canonical innate immune-mediated inflammatory responses (or immune-dependent signaling-induced responses), molecules of the innate immune system regulate pathophysiological responses in multiple organs during metabolic disturbances (termed immune-independent signaling-induced responses), including the disruption of metabolic homeostasis, tissue repair, and cell survival. In addition, emerging evidence from the study of immunometabolism indicates that the systemic metabolic status may have profound effects on cellular immune function and phenotypes through the alteration of cell-intrinsic metabolism. We summarize how the innate immune system interacts with metabolic disturbances to trigger immune-dependent and immune-independent pathogenesis in the context of nonalcoholic fatty liver disease, as representative of metabolic diseases, and cardiovascular diseases.


Hepatology ◽  
2013 ◽  
Vol 58 (1) ◽  
pp. 128-138 ◽  
Author(s):  
Angelina Mouralidarane ◽  
Junpei Soeda ◽  
Clara Visconti-Pugmire ◽  
Anne-Maj Samuelsson ◽  
Joaquim Pombo ◽  
...  

2021 ◽  
Vol 8 ◽  
Author(s):  
Juqiang Han ◽  
Xiang Zhang

Non-alcoholic fatty liver disease (NAFLD) is currently the most common cause of chronic liver disorder worldwide. The pathological spectrum of NAFLD ranges from simple steatosis to non-alcoholic steatohepatitis (NASH) that induces progressive liver cirrhosis and eventually hepatocellular carcinoma (HCC). However, the molecular mechanisms driving the transformation of NASH are obscure. There is a compelling need for understanding the pathogenic mechanisms of NASH, and thereby providing new insight into mechanism-based therapy. Currently, several studies reported that complement system, an innate immune system, played an important role in the pathogenesis of NAFLD, which was also proved by our recent study. Complement component 3 (C3), a protein of the innate immune system, plays a hub role in the complement system. Herein, we present a review on the role and molecular mechanism of C3 in NASH as well as its implication in NASH diagnosis and treatment.


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