scholarly journals Role of hepatic macrophages in alcoholic liver disease

2016 ◽  
Vol 64 (6) ◽  
pp. 1075-1077 ◽  
Author(s):  
Cynthia Ju ◽  
Suthat Liangpunsakul
Keyword(s):  
Liver Disease ◽  
Alcohol Consumption ◽  
Immune Responses ◽  
Alcoholic Liver Disease ◽  
Phenotypic Diversity ◽  
Critical Role ◽  
Gut Permeability ◽  
Hepatic Macrophages ◽  
Translocation Of Bacteria

Alcohol consumption can lead to the increase in gut permeability and cause the translocation of bacteria-derived lipopolysaccharides from the gut to the liver, which subsequently activates immune responses. In this process, macrophages play a critical role and involve in the pathogenesis of alcoholic liver disease (ALD). To define the mechanism underpinning the function of macrophages, it is important to conduct extensive studies to further explicate the phenotypic diversity of macrophages in the context of ALD. In this review, the role of hepatic macrophages in the pathogenesis of ALD is discussed.

scholarly journals Innate immunity in alcoholic liver disease

2011 ◽  
Vol 300 (4) ◽  
pp. G516-G525 ◽  
Author(s):  
Bin Gao ◽  
Ekihiro Seki ◽  
David A. Brenner ◽  
Scott Friedman ◽  
Jessica I. Cohen ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Liver Disease ◽  
Alcohol Consumption ◽  
Liver Fibrosis ◽  
Alcoholic Liver Disease ◽  
Chronic Viral Hepatitis ◽  
Western World ◽  
Excessive Alcohol Consumption ◽  
Alcoholic Steatohepatitis

Excessive alcohol consumption is a leading cause of chronic liver disease in the Western world. Alcohol-induced hepatotoxicity and oxidative stress are important mechanisms contributing to the pathogenesis of alcoholic liver disease. However, emerging evidence suggests that activation of innate immunity involving TLR4 and complement also plays an important role in initiating alcoholic steatohepatitis and fibrosis, but the role of adaptive immunity in the pathogenesis of alcoholic liver disease remains obscure. Activation of a TLR4-mediated MyD88-independent (TRIF/IRF-3) signaling pathway in Kupffer cells contributes to alcoholic steatohepatitis, whereas activation of TLR4 signaling in hepatic stellate cells promotes liver fibrosis. Alcohol consumption activates the complement system in the liver by yet unidentified mechanisms, leading to alcoholic steatohepatitis. In contrast to activation of TLR4 and complement, alcohol consumption can inhibit natural killer cells, another important innate immunity component, contributing to alcohol-mediated acceleration of viral infection and liver fibrosis in patients with chronic viral hepatitis. Understanding of the role of innate immunity in the pathogenesis of alcoholic liver disease may help us identify novel therapeutic targets to treat this disease.

scholarly journals The critical role of toll-like receptor (TLR) 4 in alcoholic liver disease is independent of the common TLR adapter MyD88

Hepatology ◽  
2008 ◽  
Vol 48 (4) ◽  
pp. 1224-1231 ◽  
Author(s):  
Istvan Hritz ◽  
Pranoti Mandrekar ◽  
Arumugam Velayudham ◽  
Donna Catalano ◽  
Angela Dolganiuc ◽  
...  
Keyword(s):  
Liver Disease ◽  
Alcoholic Liver Disease ◽  
Critical Role ◽  
Toll Like Receptor ◽  
The Common

scholarly journals Alcoholic-Hepatitis, Links to Brain and Microbiome: Mechanisms, Clinical and Experimental Research

Biomedicines ◽  
2020 ◽  
Vol 8 (3) ◽  
pp. 63
Author(s):  
Manuela G. Neuman ◽  
Helmut Karl Seitz ◽  
Samuel W. French ◽  
Stephen Malnick ◽  
Heidekazu Tsukamoto ◽  
...  
Keyword(s):  
Liver Disease ◽  
Alcohol Consumption ◽  
Immune Responses ◽  
Alcoholic Hepatitis ◽  
Liver Steatosis ◽  
Hepatocellular Cancer ◽  
Organ Damage ◽  
Experimental Models ◽  
T Helper 17

The following review article presents clinical and experimental features of alcohol-induced liver disease (ALD). Basic aspects of alcohol metabolism leading to the development of liver hepatotoxicity are discussed. ALD includes fatty liver, acute alcoholic hepatitis with or without liver failure, alcoholic steatohepatitis (ASH) leading to fibrosis and cirrhosis, and hepatocellular cancer (HCC). ALD is fully attributable to alcohol consumption. However, only 10–20% of heavy drinkers (persons consuming more than 40 g of ethanol/day) develop clinical ALD. Moreover, there is a link between behaviour and environmental factors that determine the amount of alcohol misuse and their liver disease. The range of clinical presentation varies from reversible alcoholic hepatic steatosis to cirrhosis, hepatic failure, and hepatocellular carcinoma. We aimed to (1) describe the clinico-pathology of ALD, (2) examine the role of immune responses in the development of alcoholic hepatitis (ASH), (3) propose diagnostic markers of ASH, (4) analyze the experimental models of ALD, (5) study the role of alcohol in changing the microbiota, and (6) articulate how findings in the liver and/or intestine influence the brain (and/or vice versa) on ASH; (7) identify pathways in alcohol-induced organ damage and (8) to target new innovative experimental concepts modeling the experimental approaches. The present review includes evidence recognizing the key toxic role of alcohol in ALD severity. Cytochrome p450 CYP2E1 activation may change the severity of ASH. The microbiota is a key element in immune responses, being an inducer of proinflammatory T helper 17 cells and regulatory T cells in the intestine. Alcohol consumption changes the intestinal microbiota and influences liver steatosis and liver inflammation. Knowing how to exploit the microbiome to modulate the immune system might lead to a new form of personalized medicine in ALF and ASH.

Alcohol consumption patterns in heavy drinkers with and without alcoholic liver disease (ALD)

2001 ◽  
Vol 120 (5) ◽  
pp. A117-A117
Author(s):  
K DEAR ◽  
M BRADLEY ◽  
K MCCORMACK ◽  
R PECK ◽  
D GLEESON
Keyword(s):  
Liver Disease ◽  
Alcohol Consumption ◽  
Alcoholic Liver Disease ◽  
Consumption Patterns ◽  
Heavy Drinkers

scholarly journals Overview of Non-Alcoholic Fatty Liver Disease (NAFLD) and the Role of Sugary Food Consumption and Other Dietary Components in Its Development

Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1442
Author(s):  
Pau Vancells Lujan ◽  
Esther Viñas Esmel ◽  
Emilio Sacanella Meseguer
Keyword(s):  
Clinical Trials ◽  
Liver Disease ◽  
Critical Role ◽  
Dietary Treatment ◽  
Dietary Interventions ◽  
Lifestyle Modifications ◽  
Alcoholic Fatty Liver ◽  
Effective Form ◽  
Unhealthy Diet

NAFLD is the world’s most common chronic liver disease, and its increasing prevalence parallels the global rise in diabetes and obesity. It is characterised by fat accumulation in the liver evolving to non-alcoholic steatohepatitis (NASH), an inflammatory subtype that can lead to liver fibrosis and cirrhosis. Currently, there is no effective pharmacotherapeutic treatment for NAFLD. Treatment is therefore based on lifestyle modifications including changes to diet and exercise, although it is unclear what the most effective form of intervention is. The aim of this review, then, is to discuss the role of specific nutrients and the effects of different dietary interventions on NAFLD. It is well established that an unhealthy diet rich in calories, sugars, and saturated fats and low in polyunsaturated fatty acids, fibre, and micronutrients plays a critical role in the development and progression of this disease. However, few clinical trials have evaluated the effects of nutrition interventions on NAFLD. We, therefore, summarise what is currently known about the effects of macronutrients, foods, and dietary patterns on NAFLD prevention and treatment. Most current guidelines recommend low-calorie, plant-based diets, such as the Mediterranean diet, as the most effective dietary pattern to treat NAFLD. More clinical trials are required, however, to identify the best evidence-based dietary treatment approach.

scholarly journals Critical role of the IgM Fc receptor in IgM homeostasis, B-cell survival, and humoral immune responses

2012 ◽  
Vol 109 (40) ◽  
pp. E2699-E2706 ◽  
Author(s):  
R. Ouchida ◽  
H. Mori ◽  
K. Hase ◽  
H. Takatsu ◽  
T. Kurosaki ◽  
...  
Keyword(s):  
Immune Responses ◽  
B Cell ◽  
Cell Survival ◽  
Critical Role ◽  
Fc Receptor ◽  
Humoral Immune ◽  
Humoral Immune Responses ◽  
B Cell Survival
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