Alcoholic-Hepatitis, Links to Brain and Microbiome: Mechanisms, Clinical and Experimental Research.
CYP 1A2
CYP2E1
acetaldehyde dehydrogenase (ALDH), alcohol dehydrogenase (ADH), CYP 1A1
alcoholic hepatitis
hepato-carcinogenesis
hepatocytotoxicity
his3-Δ3′ and his3- Δ5′
laboratory markers
microsomal ethanol oxidizing system (MEOS), immunohistochemistry
mithocondrion
Journal
Biomedicines
ISSN: 2227-9059
Titre abrégé: Biomedicines
Pays: Switzerland
ID NLM: 101691304
Informations de publication
Date de publication:
18 Mar 2020
18 Mar 2020
Historique:
received:
21
01
2020
revised:
02
03
2020
accepted:
09
03
2020
entrez:
22
3
2020
pubmed:
22
3
2020
medline:
22
3
2020
Statut:
epublish
Résumé
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.
Identifiants
pubmed: 32197424
pii: biomedicines8030063
doi: 10.3390/biomedicines8030063
pmc: PMC7148515
pii:
doi:
Types de publication
Journal Article
Review
Langues
eng
Subventions
Organisme : NIAAA NIH HHS
ID : R01 AA017626
Pays : United States
Organisme : NIAAA NIH HHS
ID : R01 AA026764
Pays : United States
Organisme : NIAAA NIH HHS
ID : R24 AA013162
Pays : United States
Organisme : NIEHS NIH HHS
ID : R21 ES015954
Pays : United States
Organisme : NIDA NIH HHS
ID : P30 DA044223
Pays : United States
Organisme : NIAAA NIH HHS
ID : P50 AA011999
Pays : United States
Organisme : NIAAA NIH HHS
ID : P50 AA024333
Pays : United States
Organisme : NIEHS NIH HHS
ID : R15 ES023685
Pays : United States
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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