Common immunological and cellular pathways of human alcoholic hepatitis and murine models of alcohol consumption

2018 ◽  
Vol 68 ◽  
pp. S128-S129
Author(s):  
A. Vogle ◽  
E. Burnett ◽  
H. Fey ◽  
C. Aloman
Keyword(s):  
Alcohol Consumption ◽  
Alcoholic Hepatitis ◽  
Murine Models ◽  
Cellular Pathways ◽  
Human Alcoholic

scholarly journals Restricted immunological and cellular pathways are shared by murine models of chronic alcohol consumption

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Alyx Vogle ◽  
Tongqi Qian ◽  
Shijia Zhu ◽  
Elizabeth Burnett ◽  
Holger Fey ◽  
...  
Keyword(s):  
Alcohol Consumption ◽  
Chronic Alcohol ◽  
Murine Models ◽  
Chronic Alcohol Consumption ◽  
Cellular Pathways

scholarly journals Posttraumatic Stress Disorder in Patients with Heavy Alcohol Consumption and Alcoholic Hepatitis

2018 ◽  
Vol 42 (10) ◽  
pp. 1933-1938 ◽  
Author(s):  
Niharika Samala ◽  
Spencer G. Lourens ◽  
Vijay H. Shah ◽  
Patrick S. Kamath ◽  
Arun J. Sanyal ◽  
...  
Keyword(s):  
Posttraumatic Stress Disorder ◽  
Alcohol Consumption ◽  
Posttraumatic Stress ◽  
Alcoholic Hepatitis ◽  
Stress Disorder ◽  
Heavy Alcohol ◽  
Heavy Alcohol Consumption

scholarly journals Upregulation of BRCA1 and BRCA2 in Human Alcoholic Hepatitis and Nonalcoholic Steatohepatitis

2015 ◽  
Vol 144 (suppl 2) ◽  
pp. A379-A379
Author(s):  
Guanghong Liao ◽  
Barbara French ◽  
Hui Liu ◽  
Samuel French
Keyword(s):  
Nonalcoholic Steatohepatitis ◽  
Alcoholic Hepatitis ◽  
Brca1 And Brca2 ◽  
Human Alcoholic

The Amount of Alcohol Consumption Negatively Impacts Short-Term Mortality in Mexican Patients With Alcoholic Hepatitis

2011 ◽  
Vol 106 (8) ◽  
pp. 1472-1480 ◽  
Author(s):  
José Altamirano ◽  
Fátima Higuera-de laTijera ◽  
Andres Duarte-Rojo ◽  
Manuel A Martínez-Vázquez ◽  
Juan G Abraldes ◽  
...  
Keyword(s):  
Alcohol Consumption ◽  
Alcoholic Hepatitis ◽  
Short Term ◽  
Short Term Mortality ◽  
Mexican Patients

Fatty liver disease in children

2011 ◽  
Author(s):  
R. Mark Beattie ◽  
Anil Dhawan ◽  
John W.L. Puntis
Keyword(s):  
Liver Disease ◽  
Alcohol Consumption ◽  
Liver Injury ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Alcoholic Hepatitis ◽  
Alcoholic Fatty Liver ◽  
End Stage Liver Disease ◽  
End Stage ◽  
Alcoholic Fatty Liver Disease

Demographics 406Pathophysiology 406Differential diagnoses 407Presenting features 407Investigation 408Management 409Fatty liver disease is now increasingly recognized in children, particularly in the setting of obesity.The term non-alcoholic steatohepatitis (NASH) was first coined in 1980 by Ludwig to describe a pattern of liver injury in adults in which the liver histology was consistent with alcoholic hepatitis, but in whom significant alcohol consumption was denied. NASH can be considered as part of a broader spectrum of non-alcoholic fatty liver disease that extends from simple steatosis through steatohepatitis that is characterized by the potential to progress to fibrosis, cirrhosis and subsequent end stage liver disease....

scholarly journals Murine Models of Nonalcoholic Fatty Liver Disease and Steatohepatitis

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Masashi Ninomiya ◽  
Yasuteru Kondo ◽  
Tooru Shimosegawa
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Fatty Liver Disease ◽  
Alcoholic Hepatitis ◽  
Murine Models ◽  
Excessive Alcohol Consumption ◽  
Nonalcoholic Fatty Liver ◽  
History Of ◽  
Excessive Alcohol ◽  
Multiple Hit

In 1980, Ludwig et al. first reported patients of steatohepatitis who lacked a history of excessive alcohol consumption but showed liver histology resembling alcoholic hepatitis and progression to cirrhosis of the liver accompanied by inflammation and fibrosis. The development of nonalcoholic steatohepatitis (NASH) is associated with obesity, diabetes mellitus, insulin resistance, and hyperlipidemia. However, the pathogenesis of NASH remains incomplete. A “multiple-hit” hypothesis for the pathogenesis of NASH based on an animal model has been proposed and remains a foundation for research in this field. We review the important dietary and genetic animal models and discuss the pathogenesis of NASH.

scholarly journals Murine Models of Acute Alcoholic Hepatitis and Their Relevance to Human Disease

2016 ◽  
Vol 186 (4) ◽  
pp. 748-760 ◽  
Author(s):  
Richard J.W. Wilkin ◽  
Patricia F. Lalor ◽  
Richard Parker ◽  
Philip N. Newsome
Keyword(s):  
Human Disease ◽  
Alcoholic Hepatitis ◽  
Murine Models ◽  
Acute Alcoholic Hepatitis

scholarly journals Lessons from Keratin 18 Knockout Mice: Formation of Novel Keratin Filaments, Secondary Loss of Keratin 7 and Accumulation of Liver-specific Keratin 8-Positive Aggregates

1998 ◽  
Vol 140 (6) ◽  
pp. 1441-1451 ◽  
Author(s):  
Thomas M. Magin ◽  
Rolf Schröder ◽  
Sabine Leitgeb ◽  
Frederique Wanninger ◽  
Kurt Zatloukal ◽  
...  
Keyword(s):  
Knockout Mice ◽  
Alcoholic Hepatitis ◽  
Liver Pathology ◽  
Secondary Loss ◽  
Mallory Bodies ◽  
Keratin Filaments ◽  
Keratin 18 ◽  
Keratin 7 ◽  
Human Alcoholic

Here, we report on the analysis of keratin 18 null mice. Unlike the ablation of K8, which together with K18 is expressed in embryonic and simple adult epithelia, K18 null mice are viable, fertile, and show a normal lifespan. In young K18 null mice, hepatocytes were completely devoid of keratin filaments. Nevertheless, typical desmosomes were formed and maintained. Old K18 null mice, however, developed a distinctive liver pathology with abnormal hepatocytes containing K8-positive aggregates. These stained positively for ubiquitin and MM120-1 and were identified as Mallory bodies, one hallmark of human alcoholic hepatitis. This is the first demonstration that the ablation of one keratin leads to the accumulation of its single partner. Another striking finding was the absence or drastic down regulation of K7 in several tissues despite its ongoing transcription. Moreover, K18 null mice revealed new insights in the filament-forming capacity of the tail-less K19 in vivo. Due to the unexpected secondary loss of K7, only K8/19 are expressed in the uterine epithelium of K18 null mice. Immunoelectron microscopy of this tissue demonstrated the presence of typical K8/19 IF, thus highlighting in vivo that K19 is a fully competent partner for K8.

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