scholarly journals Persistent deficiency of mucosa-associated invariant T (MAIT) cells during alcohol-related liver disease

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yujue Zhang ◽  
Yuanyuan Fan ◽  
Wei He ◽  
Yi Han ◽  
Huarui Bao ◽  
...  
Keyword(s):  
Liver Disease ◽  
Inflammatory Diseases ◽  
Alcoholic Cirrhosis ◽  
Serum Levels ◽  
Pathological Feature ◽  
Alcoholic Fatty Liver ◽  
Functional Changes ◽  
Mait Cells ◽  
Related Liver Disease ◽  
Mait Cell

Abstract Background Alcohol-related liver disease (ALD) is a major cause of chronic liver diseases. Inflammatory response is a basic pathological feature of ALD. Mucosal-associated invariant T(MAIT) cells are a novel population of innate immune cells, which may be depleted in various inflammatory diseases. However, the changes of MAIT cell in ALD remains unclear. Results In this study, the levels of MAIT cell were significantly decreased in patients with alcoholic fatty liver disease, alcoholic cirrhosis, and mixed cirrhosis (alcoholic + viral). Furthermore, the reduction of circulating MAIT cells was correlated with liver function in patients with cirrhosis. Functional changes among circulating MAIT cells in patients with alcoholic cirrhosis, including increased production of IL-17A and perforin, and reduced production of TNF-α. Plasma cytokine and chemokine levels were quantified using multiple immunoassays and ELISA. Serum levels of chemokine IL-8 were correlated with MAIT cell frequency in patients with alcoholic cirrhosis. Moreover, no differences were observed in the expression of CCR6, CXCR6, and PD-1 in circulating MAIT cells of patients with alcoholic cirrhosis. The MAIT cells in patients with alcoholic cirrhosis were prone to apoptosis, which was promoted by IL-12, IL-18, and IL-8. Conclusions Our findings indicate persistent MAIT cell loss during alcohol-related liver disease and suggest that MAIT cells can be promising indicator and therapeutic targets in ALD.

Persistent Deficiency of Mucosa-associated Invariant T (MAIT) cells During Alcohol-related Liver Disease

2021 ◽  
Author(s):  
Yujue Zhang ◽  
Yuanyuan Fan ◽  
Wei He ◽  
Yi Han ◽  
Huarui Bao ◽  
...  
Keyword(s):  
Liver Disease ◽  
Inflammatory Diseases ◽  
Alcoholic Cirrhosis ◽  
Cell Loss ◽  
Pathological Feature ◽  
Alcoholic Fatty Liver ◽  
Functional Changes ◽  
Mait Cells ◽  
Related Liver Disease ◽  
Mait Cell

Abstract Background: Alcohol-related liver disease (ALD) is a major cause of chronic liver diseases, and the inflammatory response is a basic pathological feature of ALD. Immunity throughout different stages of ALD has not yet been elucidated. The mucosal-associated invariant T(MAIT) cells are a novel population of innate immune cells, which may be depleted in various inflammatory diseases. However, the mechanism of MAIT cell loss in ALD remains unclear.Results: In this study, we found that MAIT cells were depleted in patients with alcoholic fatty liver disease, alcoholic cirrhosis, and mixed cirrhosis (alcoholic + viral). Furthermore, the reduction in circulating MAIT cells was correlated with liver function in patients with cirrhosis. We detected functional changes among circulating MAIT cells in patients with alcoholic cirrhosis, including increased production of IL-17A and perforin, and reduced production of TNF-α. Plasma cytokine and chemokine levels were quantified using multiple immunoassays and ELISA. Serum levels of chemokine IL-8 were correlated with MAIT cell frequency in patients with alcoholic cirrhosis. Moreover, no differences were observed in the expression of CCR6, CXCR6, and PD-1 in circulating MAIT cells of patients with alcoholic cirrhosis. The MAIT cells in patients with alcoholic cirrhosis were prone to apoptosis, which was promoted by IL-12, IL-18, and IL-8. Conclusions: Our findings indicate persistent MAIT cell loss during alcohol-related liver disease, and suggest that MAIT cells can be promising indicator and therapeutic targets in ALD.

Non-Alcoholic Fatty Liver Disease in Overweight Children and its Relationship with Retinol Serum Levels

2008 ◽  
Vol 78 (1) ◽  
pp. 27-32 ◽  
Author(s):  
Suano de Souza ◽  
Silverio Amancio ◽  
Saccardo Sarni ◽  
Sacchi Pitta ◽  
Fernandes ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Lipid Profile ◽  
Fatty Liver Disease ◽  
Thiobarbituric Acid ◽  
Serum Levels ◽  
Control Group ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

Objectives: To evaluate the frequency of non-alcoholic fatty liver disease, the retinol serum levels, lipid profile, and insulin resistance in overweight/obese children. To relate these biochemical variables with the risk of this disease in the population studied. Methods: The study was cross-sectional and prospective, with 46 overweight/obese school children (28 female, 18 male; mean age 8.6 years). The control group consisted of 45 children, paired by age and gender. Hepatic steatosis, evaluated by ultrasound, was classified as normal, mild, moderate, or severe. Also evaluated were serum retinol levels; thiobarbituric acid reactive substances; lipid profile; and fasting glucose and serum insulin levels, used for the calculation of the Homeostasis Model Assessment. Results: Hepatic ultrasound alterations were found in 56.5% and 48,9% of the overweight/obese and control group children, respectively. Presence of obesity was associated with high levels of triglycerides (OR = 4.6; P = 0.002). In the studied children, the risk of steatosis was related to a trend to a higher percentage of retinol inadequacy (OR = 2.8; p = 0.051); there was no association with thiobarbituric acid reactive substances, lipid profile, or insulin resistance. Conclusions: The high frequency of non-alcoholic fatty liver disease in both groups, evaluated by hepatic ultrasound, in low-socioeconomic level children, independent of nutritional condition and without significant association with insulin resistance, emphasizes that especially in developing countries, other risk factors such as micronutrient deficiencies (e.g. vitamin A) are involved.

Serum levels of hepatoprotective peptide adiponectin in non-alcoholic fatty liver disease

2006 ◽  
Vol 18 (2) ◽  
pp. 175-180 ◽  
Author(s):  
Cem Aygun ◽  
Omer Senturk ◽  
Saadettin Hulagu ◽  
Suleyman Uraz ◽  
Altay Celebi ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Serum Levels ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

scholarly journals Relationship of Non Alcoholic Fatty Liver Disease (NAFLD) and Serum Level of Thyroid Stimulating Hormone (TSH) in Normal Reference Range

2021 ◽  
pp. 33-39
Author(s):  
Doaa Ameen Khalil ◽  
Yasser Mohammed Abdul Raouf ◽  
Amal Said Al-Bendary ◽  
Kamal Mohamed Okasha
Keyword(s):  
Risk Factor ◽  
Liver Disease ◽  
Serum Level ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Independent Risk Factor ◽  
Serum Levels ◽  
Thyroid Stimulating Hormone ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

Background: Non-alcoholic fatty liver disease (NAFLD) can increase the incidence of cardiovascular disease and hepatocellular carcinoma. Thyroid hormones also play important roles in hepatic lipid metabolism and hepatic insulin resistance. Hypothyroidism is associated with reduced lipolysis and decreased liver uptake of free fatty acids derived from triglycerides. In recent years, the correlation between overt or subclinical hypothyroidism and NAFLD has been discussed. The relationship between NAFLD and thyroid function parameters remains unclear. Aim: We aimed to evaluate the relationship between serum level of Thyroid Stimulating Hormone (TSH) within normal reference range and Non Alcoholic fatty liver Disease (NAFLD). Subjects and Methods: This is a cross sectional case control study on 40 patients with NAFLD and a control group of 20 healthy individuals, who were attendants of Outpatient Clinic of Internal Medicine Department of Tanta University Hospitals and EL-Menshawy General Hospital from February 2018 to the end of January 2019. Results: In the present study, univariate regression analysis showed that serum levels of AST, FT3, FT4 and Anti-TPO were independent risk factors of NAFLD, while in multivariate analysis the only independent risk factor of NAFLD was Anti-TPO serum level. Conclusion: Serum levels of AST, FT3, FT4 and Anti-TPO were independent risk factors of NAFLD in univariate regression analysis, while in multivariate analysis the only independent risk factor of NAFLD was Anti-TPO serum level. Despite the positive correlation between serum TSH level and grade of NAFLD, the study didn’t show serum TSH level as independent risk factor of NAFLD.

Liver disorders

2021 ◽  
pp. 208-258
Author(s):  
Thomas Marjot
Keyword(s):  
Liver Transplantation ◽  
Liver Disease ◽  
Core Curriculum ◽  
Chronic Viral Hepatitis ◽  
Alcoholic Fatty Liver ◽  
Liver Disorders ◽  
Bacterial Peritonitis ◽  
Complications Of Cirrhosis ◽  
Related Liver Disease ◽  
Curriculum Topics

This chapter covers core curriculum topics relating to liver disorders including the anatomy, physiology, and biochemistry of the liver as it relates to disease processes. There is a focus on the investigation and management of acute hepatitis including viral, drug- and toxin-induced, and the risk stratification of patients with acute liver failure. All major chronic liver diseases are discussed including non-alcoholic fatty liver disease, autoimmune liver disease, alcohol related liver disease and chronic viral hepatitis. There is also education on managing the complications of cirrhosis including renal dysfunction, hepatic encephalopathy, variceal haemorrhage, and spontaneous bacterial peritonitis. Additional important topics covered include nutrition in liver disease, hepatocellular carcinoma, liver transplantation indications and assessment, and complications following liver transplantation. Additional curriculum material regarding liver disorders will also be covered in the mock examination chapter.

scholarly journals Alkoholos májbetegség: a genetikai-epigenetikai tényezők szerepe és az absztinencia hatása

2019 ◽  
Vol 160 (14) ◽  
pp. 524-532 ◽  
Author(s):  
Alajos Pár ◽  
Gabriella Pár
Keyword(s):  
Risk Factors ◽  
Liver Disease ◽  
Environmental Factors ◽  
Alcoholic Liver Disease ◽  
Liver Toxicity ◽  
Hepatitis Virus ◽  
Alcoholic Cirrhosis ◽  
Protective Role ◽  
Micro Rna ◽  
Alcoholic Fatty Liver

Abstract: The pathogenesis of alcoholic liver disease depends not only on the toxic effects of alcohol, but also on the complex interaction of host’s and environmental factors. Thus, the genetic pre-disposition, co-morbidities and behavioral factors all play a role in the individual variations in the disease outcomes. On the other hand, the essential part of the therapeutic strategy is the complete withdrawal of the harmful etiological agent. The present paper is devoted to overview the genetics, the environmental factors and the effects of abstinence in alcoholic liver disease. Genetic variants in two enzymes involved in the metabolism of ethanol, alcohol-dehydrogenase ADH1B *2 and aldehyde-dehydrogenase ALDH2 *2 through increasing the blood level of acetaldehyde, may play a “protective” role against alcoholism. The P450 CYP2E1 *5 c2, an inducible microsomal oxidase, upregulated by ethanol and by formation of acetaldehyde and reactive oxygen species, increases liver toxicity. Three novel gene polymorphisms – such as the patatin-like phospholipase domain-containing 3 (PNPLA3 I148M C>G), the transmembrane 6 superfamily member 2 (TM6SF2 E167K), and the membrane-bound O-acyltransferase domain-containing 7 (MB0AT7 rs641738 C>T) – have been proven as risk factors of steatosis, fibrosis and even hepatocellular carcinoma in both alcoholic and non-alcoholic fatty liver disease patients. Alcohol-induced epigenetic effects, reversible but inheritable gene expression alterations – as histon modulations, DNA methylation and micro-RNA-s – are of importance in the pathogenesis as well, and in the future, they may serve as diagnostic markers and therapeutic targets. Women are at greater risk of developing alcoholic cirrhosis, furthermore, malnutrition, obesity, diabetes, smoking, and hepatitis virus infections are also risk factors. Alcoholic liver disease should be regarded as a preventable disease. Several clinical studies revealed that abstinence may result in the regression of steatohepatitis and fibrosis, compensation of cirrhosis, improving disease outcome and increasing survival even in patients with advanced stages. Early diagnosis and multidisciplinary interventions are highly required to achieve long-term abstinence and to prevent alcoholic cirrhosis. Orv Hetil. 2019; 160(14): 524–532.

scholarly journals The Emerging Relevance of AIM2 in Liver Disease

2020 ◽  
Vol 21 (18) ◽  
pp. 6535
Author(s):  
Beatriz Lozano-Ruiz ◽  
José M. González-Navajas
Keyword(s):  
Liver Disease ◽  
Inflammatory Diseases ◽  
Research Area ◽  
Cellular Damage ◽  
Inflammasome Activation ◽  
Immune Recognition ◽  
Alcoholic Fatty Liver ◽  
Hepatic Diseases ◽  
Life Threatening ◽  
New Research

Absent in melanoma 2 (AIM2) is a cytosolic receptor that recognizes double-stranded DNA (dsDNA) and triggers the activation of the inflammasome cascade. Activation of the inflammasome results in the maturation of inflammatory cytokines, such as interleukin (IL)-1 β and IL-18, and a form of cell death known as pyroptosis. Owing to the conserved nature of its ligand, AIM2 is important during immune recognition of multiple pathogens. Additionally, AIM2 is also capable of recognizing host DNA during cellular damage or stress, thereby contributing to sterile inflammatory diseases. Inflammation, either in response to pathogens or due to sterile cellular damage, is at the center of the most prevalent and life-threatening liver diseases. Therefore, during the last 15 years, the study of inflammasome activation in the liver has emerged as a new research area in hepatology. Here, we discuss the known functions of AIM2 in the pathogenesis of different hepatic diseases, including non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH), hepatitis B, liver fibrosis, and hepatocellular carcinoma (HCC).

scholarly journals Bile acids serum levels in patients with nonalcoholic fatty liver disease

2015 ◽  
Vol 96 (3) ◽  
pp. 354-358 ◽  
Author(s):  
Z Sh Minnullina ◽  
S V Kiyashko ◽  
O V Ryzhkova ◽  
R G Sayfutdinov
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Bile Acids ◽  
Hepatic Steatosis ◽  
Fatty Liver Disease ◽  
Serum Levels ◽  
Healthy Individuals ◽  
Alcoholic Fatty Liver ◽  
Significant Difference ◽  
Alcoholic Fatty Liver Disease

Aim. To estimate the blood levels of primary, secondary, tertiary and unconjugated bile acids in patients with non-alcoholic fatty liver disease.Methods. The study included 74 patients with non-alcoholic fatty liver disease (males - 30, females - 44) and 51 healthy individuals (males - 14, females - 37). All patients underwent anthropometry and complete clinical, biochemical and instrumental examination (measuring the subcutaneous fat layer). 64 patients had hepatic steatosis, 10 - steatohepatitis. Serum levels of bile acids (primary: cholic, chenodeoxycholic; secondary: lithocholic, deoxycholic and tertiary: ursodeoxycholic) were measured by gas-liquid chromatography on «Chromos GC-1000» (Russia) scanner.Results. Unconjugated primary, secondary and tertiary bile acids were detected in the blood of healthy individuals and patients with non-alcoholic fatty liver disease. In healthy individuals, there were no gender differences found in the bile acids levels. Patients with non-alcoholic fatty liver disease had higher level of bile acids compared to healthy controls. There was a significant difference in the concentrations of secondary and tertiary bile acids in patients with hepatic steatosis and steatohepatitis.Conclusion. Blood bile acids levels were significantly higher in patients with non-alcoholic fatty liver disease than in healthy individuals. At steatohepatitis, females had higher levels of cholic, chenodeoxycholic and deoxycholic acids and lower levels of lithocholic and ursodeoxycholic acids compared to males. Significant difference in patients with hepatic steatosis and steatohepatitis was revealed only in levels of secondary and tertiary bile acids.

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