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Review Article | Open Access

Inflammation and gut microbiota in the alcoholic liver disease

Yan Gao1,2()
Biomedical Innovation Center, Beijing Shijitan Hospital, Capital Medical University, Beijing 100038, China
Beijing Key Laboratory for Therapeutic Cancer Vaccines, Beijing Shijitan Hospital, Capital Medical University, Beijing 100038, China
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Highlights

(1) Inflammation is essential to pathogenesis of hepatic diseases, especially inflammasome.

(2) We mainly pay close attention to the activation and function of inflammasome in ALD.

(3) After alcohol stimulation, the metabolites of gut microbiota will change, and then create a vicious cycle to liver.

Graphical Abstract

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Alcohol consumption promotes the second stroke of liver cells via action of oxidative stress-related lipid peroxidation and inflammatory cytokines, resulting into inflammatory response. Therefore, inflammasomes are multi-protein complexes which realize the risk and gather to regulate caspase-1 activation. The inflammasome activation particularly needs two signals in other to enlarge inflammation. Additionally, gut microbes are involved in the regulation of inflammation by constructing a gut specific immune system rather than reusing the infectious pathogens. After alcohol stimulation, the metabolites of gut microbiota will change, and then create a vicious cycle to liver.

Abstract

Alcoholic liver disease (ALD) covers including but not limited to oxidative stress. Alcohol, as the primary stroke, promote the second stroke of liver cells via action of oxidative stress-related lipid peroxidation and inflammatory cytokines, resulting into inflammatory response. Inflammation is essential to pathogenesis of hepatic diseases. Therefore, inflammasomes are multi-protein complexes which realize the risk and gather to regulate caspase-1 activation, activating cytokines such as interleukin-1β (IL-1β) and interleukin-18 (IL-18). Unlike inflammatory responses, the inflammasome activation particularly needs two signals in other to enlarge inflammation. It has been discovered in several human hepatic diseases and realized to be a major contributor to organic damage. Especially, we mainly pay close attention to the activation and function of inflammasome in ALD. Additionally, gut microbes are involved in the regulation of inflammation by constructing a gut specific immune system rather than reusing the infectious pathogens. Fungal flora has an auxiliary effect on inflammatory response, metabolic disorders, and bacterial microbial regulation and host defense, while alcohol abuse causes an imbalance in the microflora of human gut as the feed-back. After alcohol stimulation, the metabolites of gut microbiota will change, and then create a vicious cycle to liver. In brief, the application and translation of the current review promises new approaches in the treatment of ALD, especially from inflammasomes and gut microbiota.

Keywords

inflammasomegut microbiotaalcoholic liver diseaseshort chain fatty acidNLR family pyrin domain containing 3

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Food & Medicine Homology
Volume 1 Issue 2,
December 2024
Article number: 9420020
DOI: 10.26599/FMH.2024.9420020
Cite this article:
Gao Y. Inflammation and gut microbiota in the alcoholic liver disease. Food & Medicine Homology, 2024, 1(2): 9420020. https://doi.org/10.26599/FMH.2024.9420020
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Relative gut microbiota and metabolite function

Representative gut microbiotaMetabolitesFunctions
Firmicutes including Clostridium IV and XIVaSCFAs (acetic acid, propionic acid, butyric acid, isobutyric acid, 2-methylpropionic acid, pentanoic acid, isovalerate acid, and caproic acid)Inhibit pathogen propagation; participate in cholesterol synthesis; provide energy for epithelial cells[57-59]
Lactobacillus; Bifidobacterium; Enterobacter; Bacteroides; ClostridiumBile acid (cholate, deoxycholic acid, chenodeoxycholic acid (CDCA), muricholic acid sodium, taurocholate, ursodeoxycholic, taurodeoxycholic acid)Absorb fats and vitamins; improve fat absorption; maintain intestinal barrier function; transfer signals to regulate homeostasis[60-63]
Faecalibacterium prausnitzii; BifidobacteriumCholine metabolites (methyl amine, dimethyl amine, trimethylamine, N-trimethylamine oxide, dimethyl glycine and betaine)Regulate lipid metabolism and glucose homeostasis; participate in nonalcoholic fatty liver diseases (NAFLDs), diet-induced obesity, diabetes and cardiovascular diseases[64-66]
Clostridium difficile; Bifidobacterium; LactobacillusPhenolic, benzoyl and phenyl derivatives (benzoic acid, hippuric acid, tyrosine, styrene glycine, phenylacetylglutamine, phenylacetate, phenyl propionate, phenylpropanyl glycine and cinnamyl glycine)Detoxify exogenous substances, indicate intestinal microbial composition and activity, 4-toluene sulfate was elevated in children with serious autism
Clostridium spore; Escherichia coliIndole derivative (N-acetyl tryptophan, indole acetic acid, isoamyl gallate (IAG), indole, indole sulfuric acid, indole-3-propionic acid, melatonin, melatonin-6-sulfuric acid, serotonin and 5-hydroxyindole)Protect the gastrointestinal tract from stress induced injury, regulate the expression of pro-inflammatory gene, enhance the expression of anti-inflammatory gene, strengthen the epithelial cell barrier function; participate in gastrointestinal disease, brain-gut axis and some neural states[67-69]
Bifidobacterium bifidum; Eubacterium lentum; Veillonella; Lactobacillus; PropionibacteriumVitamins (vitamin K, vitamin B12, biotin (vitamin H), folic acid, thiamine (vitamin B1), riboflavin (vitamin B2) and vitamin B6)Offer complementary endogenous vitamins, reinforce the immune function, play epigenetic role in regulating cell proliferation, vitamin K plays a role in blood clotting, maintain normal bone metabolism, anti-arterial calcification and other functions[70-76]
Campylobacter jejuni; Clostridium thermosaccharolyticumPolyamines (putrescine, cadaverine, spermidine and spermine)Genetic toxicity of host, anti-inflammatory and anti-tumor effects, possible tumor markers[77, 78]
B. bifidum; Roseburia; Lactobacillus; Klebsiella; Enterobacter coli; Citrobacter; FusobacteriumLipids (conjugated fatty acid, LPS, peptidoglycan, acylglecerol, sphingomyelin, cholesterol, lecithin, phosphorylethanolamine and triglyceride)Intestinal permeability effects, activate the gut-brain-liver axis to mediate glucose homeostasis, LPS induces chronic systemic inflammation, combine fatty acids to improve hyperinsulinemia, promote immune system function and change lipoprotein profile, cholesterol is the foundation for production of sterols and cholic acids[79, 80]
Bacteroides; Pseudomonas butyricum; Ruminococcus; Faecalis benthos; Micrococcus; B. bifidum; LactobacillusOther metabolites (D-lactic acid, formic acid, ethanol, methanol, succinic acid, lysine, glucose, urea, α-ketoisovaleric acid, creatine, creatinine anhydride, endocannabinoids, 2-arachidonoylglycerol (2-AG), N-arachidonic ethanolamine and LPS)Direct or indirect synthesis or utilization of various compounds, including the regulation of related pathways such as the endocannabinoid system[79, 81-84]