Alcohol, Inflammation, and Microbiota in Alcoholic Liver Disease

Abstract

Alcoholic liver disease (ALD) is a consequence of excessive alcohol use. According to many studies, alcohol represents a significant socioeconomic and health risk factor in today’s population. According to data from the World Health Organization, there are about 75 million people who have alcohol disorders, and it is well known that its use leads to serious health problems. ALD is a multimodality spectrum that includes alcoholic fatty liver disease (AFL) and alcoholic steatohepatitis (ASH), consequently leading to liver fibrosis and cirrhosis. In addition, the rapid progression of alcoholic liver disease can lead to alcoholic hepatitis (AH). Alcohol metabolism produces toxic metabolites that lead to tissue and organ damage through an inflammatory cascade that includes numerous cytokines, chemokines, and reactive oxygen species (ROS). In the process of inflammation, mediators are cells of the immune system, but also resident cells of the liver, such as hepatocytes, hepatic stellate cells, and Kupffer cells. These cells are activated by exogenous and endogenous antigens, which are called pathogen and damage-associated molecular patterns (PAMPs, DAMPs). Both are recognized by Toll-like receptors (TLRs), which activation triggers the inflammatory pathways. It has been proven that intestinal dysbiosis and disturbed integrity of the intestinal barrier perform a role in the promotion of inflammatory liver damage. These phenomena are also found in chronic excessive use of alcohol. The intestinal microbiota has an important role in maintaining the homeostasis of the organism, and its role in the treatment of ALD has been widely investigated. Prebiotics, probiotics, postbiotics, and symbiotics represent therapeutic interventions that can have a significant effect on the prevention and treatment of ALD.

Establishment and validation of a predictive nomogram for severe pleural effusion in liver cancer patients after hepatectomy

“…This suggests that drinking history itself may represent broader influences. Firstly, alcohol consumption can exacerbate liver inflammation and fibrosis, [20][21][22][23][24] Inflammation leads to liver tissue damage and destruction, affecting normal liver function. Inflammatory responses also activate the release of inflammatory mediators, further increasing vascular permeability and impairing lymphatic circulation, thereby promoting pleural effusion formation.…”

The effects of BDNF rs6265 and FGF21 rs11665896 polymorphisms on alcohol use disorder-related impulsivity in Han Chinese adults

“…Long-term heavy drinking can lead to inflammation and apoptosis ( 53 , 54 ). Pro-BDNF and BDNF may produce opposite biological functions by signaling through p75NTR and TrkB, respectively ( 55 ).…”

Increased Intestinal Permeability and Decreased Resiliency of the Intestinal Barrier in Alcoholic Liver Disease

“…While the likelihood of developing ALD increases with increased alcohol consumption, extensive individual variability exists ( 7 ) indicating that while excessive alcohol consumption is necessary for the development of ALD, it alone is not sufficient in inducing ALD. Several experiment studies in animal models and human ( 11 , 12 ) have demonstrated that inflammation is required for alcohol-induced liver cell injury and clinically relevant ALD. One of the primary sources of systemic and hepatic inflammation in AUD seems to be alcohol-induced gut microbiota dysbiosis and disruption of intestinal barrier (gut leakiness to endotoxins and other proinflammatory products of gut microbiota) ( 13 , 14 ).…”