Recent advances of sterile inflammation and inter-organ cross-talk in alcoholic liver disease

Alcoholic liver disease (ALD) is one of the fastest-growing concerns worldwide. In addition to bacterial endotoxins in the portal circulation, recent lines of evidence have suggested that sterile inflammation caused by a wide range of stimuli induces alcoholic liver injury, in which damage-associate...

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Published inExperimental & molecular medicine Vol. 52; no. 5; pp. 772 - 780
Main Authors Shim, Young-Ri, Jeong, Won-Il
Format Journal Article
LanguageEnglish
Published United States Springer Nature B.V 01.05.2020
Nature Publishing Group UK
Nature Publishing Group
생화학분자생물학회
Subjects
Adipose tissue
Alcohol
Bone marrow
Cell interactions
Chemokines
Double-stranded RNA
Drug development
Endotoxins
Extracellular vesicles
Hepatocytes
Inflammation
Intestine
Kupffer cells
Lipids
Lipogenesis
Liver diseases
Metabolites
miRNA
Mitochondrial DNA
Oxidative stress
Pattern recognition receptors
Review
Stellate cells
Therapeutic applications
Therapeutic targets
Toll-like receptors
생화학
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Abstract Alcoholic liver disease (ALD) is one of the fastest-growing concerns worldwide. In addition to bacterial endotoxins in the portal circulation, recent lines of evidence have suggested that sterile inflammation caused by a wide range of stimuli induces alcoholic liver injury, in which damage-associated molecular patterns (DAMPs) play critical roles in inducing de novo lipogenesis and inflammation through the activation of cellular pattern recognition receptors such as Toll-like receptors in non-parenchymal cells. Interestingly, alcohol-mediated metabolic, neurological, and immune stresses stimulate the generation of DAMPs that are released not only in the liver, but also in other organs, such as adipose tissue, intestine, and bone marrow. Thus, diverse DAMPs, including retinoic acids, proteins, lipids, microRNAs, mitochondrial DNA, and mitochondrial double-stranded RNA, contribute to a broad spectrum of ALD through the production of multiple pro-inflammatory cytokines, chemokines, and ligands in non-parenchymal cells, such as Kupffer cells, hepatic stellate cells, and various immune cells. Therefore, this review summarizes recent studies on the identification and understanding of DAMPs, their receptors, and cross-talk between the liver and other organs, and highlights successful therapeutic targets and potential strategies in drug development that can be used to combat ALD.
AbstractList Alcoholic liver disease: cross-talk with other organs Therapies preventing the distribution of damage-associated molecules from other organs to the liver could help tackle alcoholic liver disease (ALD). Over time, metabolites from excessive alcohol consumption induce oxidative stress, damaging liver cells. Injured hepatocytes release molecules known as damage-associated molecular patterns (DAMPs), including proteins, RNA, and metabolites, which disperse within the liver and other organs and trigger chronic inflammation. Won-Il Jeong and Young-Ri Shim at the Korea Advanced Institute of Science and Technology in Daejeon reviewed understanding of DAMPs to identify possible therapeutic targets for ALD. DAMPs are carried between cells by extracellular vesicles, particles released during cellular communication. Alcohol-induced DAMPs in other organs, such as the gut, can deliver to the liver, and it influences ALD progression. The more-detailed cross-talk between the liver and other organs in ALD requires further investigation.
Alcoholic liver disease (ALD) is one of the fastest-growing concerns worldwide. In addition to bacterial endotoxins in the portal circulation, recent lines of evidence have suggested that sterile inflammation caused by a wide range of stimuli induces alcoholic liver injury, in which damage-associated molecular patterns (DAMPs) play critical roles in inducing de novo lipogenesis and inflammation through the activation of cellular pattern recognition receptors such as Toll-like receptors in non-parenchymal cells. Interestingly, alcohol-mediated metabolic, neurological, and immune stresses stimulate the generation of DAMPs that are released not only in the liver, but also in other organs, such as adipose tissue, intestine, and bone marrow. Thus, diverse DAMPs, including retinoic acids, proteins, lipids, microRNAs, mitochondrial DNA, and mitochondrial double-stranded RNA, contribute to a broad spectrum of ALD through the production of multiple pro-inflammatory cytokines, chemokines, and ligands in non-parenchymal cells, such as Kupffer cells, hepatic stellate cells, and various immune cells. Therefore, this review summarizes recent studies on the identification and understanding of DAMPs, their receptors, and cross-talk between the liver and other organs, and highlights successful therapeutic targets and potential strategies in drug development that can be used to combat ALD. Therapies preventing the distribution of damage-associated molecules from other organs to the liver could help tackle alcoholic liver disease (ALD). Over time, metabolites from excessive alcohol consumption induce oxidative stress, damaging liver cells. Injured hepatocytes release molecules known as damage-associated molecular patterns (DAMPs), including proteins, RNA, and metabolites, which disperse within the liver and other organs and trigger chronic inflammation. Won-Il Jeong and Young-Ri Shim at the Korea Advanced Institute of Science and Technology in Daejeon reviewed understanding of DAMPs to identify possible therapeutic targets for ALD. DAMPs are carried between cells by extracellular vesicles, particles released during cellular communication. Alcohol-induced DAMPs in other organs, such as the gut, can deliver to the liver, and it influences ALD progression. The more-detailed cross-talk between the liver and other organs in ALD requires further investigation.
Alcoholic liver disease (ALD) is one of the fastest-growing concerns worldwide. In addition to bacterial endotoxins in the portal circulation, recent lines of evidence have suggested that sterile inflammation caused by a wide range of stimuli induces alcoholic liver injury, in which damage-associated molecular patterns (DAMPs) play critical roles in inducing de novo lipogenesis and inflammation through the activation of cellular pattern recognition receptors such as Toll-like receptors in non-parenchymal cells. Interestingly, alcohol-mediated metabolic, neurological, and immune stresses stimulate the generation of DAMPs that are released not only in the liver, but also in other organs, such as adipose tissue, intestine, and bone marrow. Thus, diverse DAMPs, including retinoic acids, proteins, lipids, microRNAs, mitochondrial DNA, and mitochondrial double-stranded RNA, contribute to a broad spectrum of ALD through the production of multiple pro-inflammatory cytokines, chemokines, and ligands in non-parenchymal cells, such as Kupffer cells, hepatic stellate cells, and various immune cells. Therefore, this review summarizes recent studies on the identification and understanding of DAMPs, their receptors, and cross-talk between the liver and other organs, and highlights successful therapeutic targets and potential strategies in drug development that can be used to combat ALD.Alcoholic liver disease: cross-talk with other organsTherapies preventing the distribution of damage-associated molecules from other organs to the liver could help tackle alcoholic liver disease (ALD). Over time, metabolites from excessive alcohol consumption induce oxidative stress, damaging liver cells. Injured hepatocytes release molecules known as damage-associated molecular patterns (DAMPs), including proteins, RNA, and metabolites, which disperse within the liver and other organs and trigger chronic inflammation. Won-Il Jeong and Young-Ri Shim at the Korea Advanced Institute of Science and Technology in Daejeon reviewed understanding of DAMPs to identify possible therapeutic targets for ALD. DAMPs are carried between cells by extracellular vesicles, particles released during cellular communication. Alcohol-induced DAMPs in other organs, such as the gut, can deliver to the liver, and it influences ALD progression. The more-detailed cross-talk between the liver and other organs in ALD requires further investigation.
Alcoholic liver disease (ALD) is one of the fastest-growing concerns worldwide. In addition to bacterial endotoxins in the portal circulation, recent lines of evidence have suggested that sterile inflammation caused by a wide range of stimuli induces alcoholic liver injury, in which damage-associated molecular patterns (DAMPs) play critical roles in inducing de novo lipogenesis and inflammation through the activation of cellular pattern recognition receptors such as Toll-like receptors in non-parenchymal cells. Interestingly, alcohol-mediated metabolic, neurological, and immune stresses stimulate the generation of DAMPs that are released not only in the liver, but also in other organs, such as adipose tissue, intestine, and bone marrow. Thus, diverse DAMPs, including retinoic acids, proteins, lipids, microRNAs, mitochondrial DNA, and mitochondrial double-stranded RNA, contribute to a broad spectrum of ALD through the production of multiple pro-inflammatory cytokines, chemokines, and ligands in non-parenchymal cells, such as Kupffer cells, hepatic stellate cells, and various immune cells. Therefore, this review summarizes recent studies on the identification and understanding of DAMPs, their receptors, and cross-talk between the liver and other organs, and highlights successful therapeutic targets and potential strategies in drug development that can be used to combat ALD. KCI Citation Count: 0
Alcoholic liver disease (ALD) is one of the fastest-growing concerns worldwide. In addition to bacterial endotoxins in the portal circulation, recent lines of evidence have suggested that sterile inflammation caused by a wide range of stimuli induces alcoholic liver injury, in which damage-associated molecular patterns (DAMPs) play critical roles in inducing de novo lipogenesis and inflammation through the activation of cellular pattern recognition receptors such as Toll-like receptors in non-parenchymal cells. Interestingly, alcohol-mediated metabolic, neurological, and immune stresses stimulate the generation of DAMPs that are released not only in the liver, but also in other organs, such as adipose tissue, intestine, and bone marrow. Thus, diverse DAMPs, including retinoic acids, proteins, lipids, microRNAs, mitochondrial DNA, and mitochondrial double-stranded RNA, contribute to a broad spectrum of ALD through the production of multiple pro-inflammatory cytokines, chemokines, and ligands in non-parenchymal cells, such as Kupffer cells, hepatic stellate cells, and various immune cells. Therefore, this review summarizes recent studies on the identification and understanding of DAMPs, their receptors, and cross-talk between the liver and other organs, and highlights successful therapeutic targets and potential strategies in drug development that can be used to combat ALD.
Abstract Alcoholic liver disease (ALD) is one of the fastest-growing concerns worldwide. In addition to bacterial endotoxins in the portal circulation, recent lines of evidence have suggested that sterile inflammation caused by a wide range of stimuli induces alcoholic liver injury, in which damage-associated molecular patterns (DAMPs) play critical roles in inducing de novo lipogenesis and inflammation through the activation of cellular pattern recognition receptors such as Toll-like receptors in non-parenchymal cells. Interestingly, alcohol-mediated metabolic, neurological, and immune stresses stimulate the generation of DAMPs that are released not only in the liver, but also in other organs, such as adipose tissue, intestine, and bone marrow. Thus, diverse DAMPs, including retinoic acids, proteins, lipids, microRNAs, mitochondrial DNA, and mitochondrial double-stranded RNA, contribute to a broad spectrum of ALD through the production of multiple pro-inflammatory cytokines, chemokines, and ligands in non-parenchymal cells, such as Kupffer cells, hepatic stellate cells, and various immune cells. Therefore, this review summarizes recent studies on the identification and understanding of DAMPs, their receptors, and cross-talk between the liver and other organs, and highlights successful therapeutic targets and potential strategies in drug development that can be used to combat ALD.
Author Jeong, Won-Il
Shim, Young-Ri
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  organization: Laboratory of Liver Research, Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon, Korea. wijeong@kaist.ac.kr
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PublicationDate_xml – month: 05
  year: 2020
  text: 2020-05-01
  day: 01
PublicationDecade 2020
PublicationPlace United States
PublicationPlace_xml – name: United States
– name: Seoul
– name: London
PublicationTitle Experimental & molecular medicine
PublicationTitleAlternate Exp Mol Med
PublicationYear 2020
Publisher Springer Nature B.V
Nature Publishing Group UK
Nature Publishing Group
생화학분자생물학회
Publisher_xml – name: Springer Nature B.V
– name: Nature Publishing Group UK
– name: Nature Publishing Group
– name: 생화학분자생물학회
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Snippet Alcoholic liver disease (ALD) is one of the fastest-growing concerns worldwide. In addition to bacterial endotoxins in the portal circulation, recent lines of...
Abstract Alcoholic liver disease (ALD) is one of the fastest-growing concerns worldwide. In addition to bacterial endotoxins in the portal circulation, recent...
Alcoholic liver disease: cross-talk with other organs Therapies preventing the distribution of damage-associated molecules from other organs to the liver could...
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SubjectTerms Adipose tissue
Alcohol
Bone marrow
Cell interactions
Chemokines
Double-stranded RNA
Drug development
Endotoxins
Extracellular vesicles
Hepatocytes
Inflammation
Intestine
Kupffer cells
Lipids
Lipogenesis
Liver diseases
Metabolites
miRNA
Mitochondrial DNA
Oxidative stress
Pattern recognition receptors
Review
Stellate cells
Therapeutic applications
Therapeutic targets
Toll-like receptors
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Title Recent advances of sterile inflammation and inter-organ cross-talk in alcoholic liver disease
URI https://www.ncbi.nlm.nih.gov/pubmed/32457490
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