scholarly journals Regulatory T cells suppress excessive lipid accumulation in alcoholic liver disease

2019 ◽  
Vol 60 (5) ◽  
pp. 922-936 ◽  
Author(s):  
Hongwu Wang ◽  
Ting Wu ◽  
Yaqi Wang ◽  
Xiaoyang Wan ◽  
Junying Qi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
T Cells ◽  
Liver Disease ◽  
Alcohol Consumption ◽  
Regulatory T Cells ◽  
Alcoholic Liver Disease ◽  
Lipid Accumulation ◽  
Chronic Alcohol ◽  
Chronic Alcohol Consumption ◽  
Alcoholic Fatty Liver

Sensitization of hepatic immune cells from chronic alcohol consumption gives rise to inflammatory accumulation, which is considered a leading cause of liver damage. Regulatory T cells (Tregs) are an immunosuppressive cell subset that plays an important role in a variety of liver diseases; however, data about pathological involvement of Tregs in liver steatosis of alcoholic liver disease (ALD) is insufficient. In mouse models of ALD, we found that increased lipid accumulation by chronic alcohol intake was accompanied by oxidative stress, inflammatory accumulation, and Treg decline in the liver. Adoptive transfer of Tregs relieved lipid metabolic disorder, oxidative stress, inflammation, and, consequently, ameliorated the alcoholic fatty liver. Macrophages are a dominant source of inflammation in ALD. Aberrant macrophage activation and cytokine production were activated during chronic alcohol consumption, but were significantly inhibited after Treg transfer. In vitro, macrophages were co-activated by alcohol and lipopolysaccharide to mimic a condition for alcoholic liver microenvironment. Tregs suppressed monocyte chemoattractant protein-1 and TNF-α production from these macrophages. However, such effects of Tregs were remarkably neutralized when interleukin (IL)-10 was blocked. Altogether, our data uncover a novel role of Tregs in restoring liver lipid metabolism in ALD, which partially relies on IL-10-mediated suppression of hepatic pro-inflammatory macrophages.

scholarly journals Withdrawal: Regulatory T cells suppress excessive lipid accumulation in alcoholic liver disease

2020 ◽  
Vol 61 (1) ◽  
pp. 127-127
Author(s):  
Hongwu Wang ◽  
Ting Wu ◽  
Yaqi Wang ◽  
Xiaoyang Wan ◽  
Junying Qi ◽  
...  
Keyword(s):  
T Cells ◽  
Liver Disease ◽  
Regulatory T Cells ◽  
Alcoholic Liver Disease ◽  
Lipid Accumulation

scholarly journals Study of clinical and biochemical profile of acute alcoholic liver disease in a teaching hospital in Telangana

2018 ◽  
Vol 5 (4) ◽  
pp. 804
Author(s):  
Shamsunder Khatroth
Keyword(s):  
Liver Disease ◽  
Alcohol Consumption ◽  
Alcoholic Liver Disease ◽  
Biochemical Parameters ◽  
Clinical Manifestations ◽  
Age Group ◽  
Biochemical Profile ◽  
Chronic Alcohol ◽  
Chronic Alcohol Consumption ◽  
Female Ratio

Background: Chronic alcohol consumption gives rise to various health risks that include liver disease, heart disease, pancreatitis, central nervous system disorders and certain forms of cancer. Alcoholic liver disease (ALD) is a spectrum of clinicopathological abnormalities, reflecting an acute or chronic inflammation of the liver parenchyma induced by alcohol use. It is associated with changes in various biochemical parameters and also various clinical manifestations in the patients. The objective of the present study to evaluate clinical and biochemical profile of acute alcoholic liver disease.Methods: The prospective hospital-based case control study was done at MNR Medical College, in the department of General Medicine for duration of one year from March 2017 to April 2018. A total of 120 cases diagnosed clinically and biochemically as Acute alcoholic liver disease were included in the study.Results: The age group ranged from 20 to 60 years and the male to female ratio was 2.42. Majority of the patients were in the age group of 30-40 years (54.1%).  Majority of the patients (66.6%) consumed >60 grams/24hours of alcohol. Jaundice, nausea and vomiting were seen in 83.3% cases followed by hepatomegaly in 66.6% cases. Majority of them had been consuming alcohol for more than 5 years.Conclusions: Chronic alcohol consumption is more common in adult males. Chronic alcoholics consume more amount of alcohol. Alcoholic liver disease has a varied clinical presentation and is associated with deranged biochemical parameters.

scholarly journals Alcohol induced hepatic retinoid depletion is associated with the induction of multiple retinoid catabolizing cytochrome P450 enzymes

PLoS ONE ◽  
2022 ◽  
Vol 17 (1) ◽  
pp. e0261675
Author(s):  
Afroza Ferdouse ◽  
Rishi R. Agrawal ◽  
Madeleine A. Gao ◽  
Hongfeng Jiang ◽  
William S. Blaner ◽  
...  
Keyword(s):  
Cytochrome P450 ◽  
Retinoic Acid ◽  
Liver Disease ◽  
Alcohol Consumption ◽  
Vitamin A ◽  
Alcohol Exposure ◽  
Chronic Alcohol ◽  
Wild Type ◽  
Chronic Alcohol Consumption ◽  
Retinyl Esters

Chronic alcohol consumption leads to a spectrum of liver disease that is associated with significant global mortality and morbidity. Alcohol is known to deplete hepatic vitamin A content, which has been linked to the pathogenesis of alcoholic liver disease. It has been suggested that induction of Cytochrome P450 2E1 (CYP2E1) contributes to alcohol-induced hepatic vitamin A depletion, but the possible contributions of other retinoid-catabolizing CYPs have not been well studied. The main objective of this study was to better understand alcohol-induced hepatic vitamin A depletion and test the hypothesis that alcohol-induced depletion of hepatic vitamin A is due to CYP-mediated oxidative catabolism. This hypothesis was tested in a mouse model of chronic alcohol consumption, including wild type and Cyp2e1 -/- mice. Our results show that chronic alcohol consumption is associated with decreased levels of hepatic retinol, retinyl esters, and retinoic acid. Moreover, the depletion of hepatic retinoid is associated with the induction of multiple retinoid catabolizing CYPs, including CYP26A1, and CYP26B1 in alcohol fed wild type mice. In Cyp2e1 -/- mice, alcohol-induced retinol decline is blunted but retinyl esters undergo a change in their acyl composition and decline upon alcohol exposure like WT mice. In conclusion, the alcohol induced decline in hepatic vitamin A content is associated with increased expression of multiple retinoid-catabolizing CYPs, including the retinoic acid specific hydroxylases CYP26A1 and CYP26B1.

scholarly journals Protective Mechanism of Edible Food Plants against Alcoholic Liver Disease with Special Mention to Polyphenolic Compounds

Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1612
Author(s):  
Liang Zhao ◽  
Arshad Mehmood ◽  
Dongdong Yuan ◽  
Muhammad Usman ◽  
Mian Anjum Murtaza ◽  
...  
Keyword(s):  
Liver Disease ◽  
Bioactive Compounds ◽  
Alcoholic Liver Disease ◽  
Alcohol Exposure ◽  
Therapeutic Interventions ◽  
Food Plants ◽  
Protective Mechanism ◽  
Chronic Alcohol ◽  
Alcoholic Fatty Liver ◽  
Main Site

Alcoholic liver disease (ALD) is one type of liver disease, causing a global healthcare problem and mortality. The liver undergoes tissue damage by chronic alcohol consumption because it is the main site for metabolism of ethanol. Chronic alcohol exposure progresses from alcoholic fatty liver (AFL) to alcoholic steatohepatitis (ASH), which further lead to fibrosis, cirrhosis, and even hepatocellular cancer. Therapeutic interventions to combat ALD are very limited such as use of corticosteroids. However, these therapeutic drugs are not effective for long-term usage. Therefore, additional effective and safe therapies to cope with ALD are urgently needed. Previous studies confirmed that edible food plants and their bioactive compounds exert a protective effect against ALD. In this review article, we summarized the hepatoprotective potential of edible food plants and their bioactive compounds. The underlying mechanism for the prevention of ALD by edible food plants was as follows: anti-oxidation, anti-inflammation, lipid regulation, inhibition of apoptosis, gut microbiota composition modulation, and anti-fibrosis.

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