Alcoholic hepatitis: The pivotal role of Kupffer cells

Suraweera, Duminda; Weeratunga, Ashley N; Hu, Robert W.; Pandol, Stephen J.; Hu, Richard

doi:10.4291/wjgp.v6.i4.90

Cited by 18 publications

(18 citation statements)

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“…In ALD patients macrophages are particularly enriched in the portal tracts and have a central role in promoting inflammation associated with ethanol-induced injury, particularly in severe alcoholic hepatitis (Ju and Mandrekar, 2015;Suraweera et al, 2015) where increased gut permeability and high portal levels of endotoxins contribute to accumulation and exacerbated activation of Ly-6C hi murine macrophages and the release of TNF, ROS and CCL2 (Petrasek et al, 2012;Wang et al, 2014;Ju and Tacke, 2016).…”

Section: Kupffer Cells and Monocyte-derived Macrophages In Cldmentioning

confidence: 99%

Liver fibrosis: Pathophysiology, pathogenetic targets and clinical issues

Parola

Pinzani

2019

Molecular Aspects of Medicine

767

605

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The progression of chronic liver diseases (CLD), irrespective of etiology, involves chronic parenchymal injury, persistent activation of inflammatory response as well as sustained activation of liver fibrogenesis and wound healing response. Liver fibrogenesis, is a dynamic, highly integrated molecular, cellular and tissue process responsible for driving the excess accumulation of extracellular matrix (ECM) components (i.e., liver fibrosis) sustained by an eterogeneous population of hepatic myofibroblasts (MFs). The process of liver fibrogenesis recognizes a number of common and etiology-independent mechanisms and events but it is also significantly influenced by the specific etiology, as also reflected by peculiar morphological patterns of liver fibrosis development. In this review we will analyze the most relevant established and/or emerging pathophysiological issues underlying CLD progression with a focus on the role of critical hepatic cell populations, mechanisms and signaling pathways involved, as they represent potential therapeutic targets, to finally analyze selected and relevant clinical issues.

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Section: Kupffer Cells and Monocyte-derived Macrophages In Cldmentioning

confidence: 99%

Liver fibrosis: Pathophysiology, pathogenetic targets and clinical issues

Parola

Pinzani

2019

Molecular Aspects of Medicine

767

605

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“…In addition, these pro-inflammatory cytokines and LPS cause the release of excess amounts of collagen and α-smooth muscle actin, which activates hepatic stellate cells and further promotes fibrosis. [36][37][38][39] Current data from animal and clinical studies point to the gut-liver axis that will bring promising results for primary or secondary prevention of HCC. The microbiome provides biomarkers to test the risk and progression of the disease.…”

Section: Discussionmentioning

confidence: 99%

Gut-microbiome Taxonomic Profiling as Non-invasive Biomarkers for the Early Detection of Alcoholic Hepatocellular Carcinoma

Seok

Suk²

2020

J Liver Cancer

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Background/Aims: Hepatocellular carcinoma (HCC) is a prevalent form of primary liver cancer and the fifth leading cause of worldwide cancer mortality. Though early diagnosis of HCC is important, so far lack of effective biomarkers for early diagnosis of HCC has been a problem. In this study, we searched for potential functional biomarkers of alcoholic HCC by using metagenomics approach. Methods: Between September 2017 and April 2019, normal control (n=44), alcoholic liver cirrhosis (n=44), and alcoholic HCC (n=13) groups were prospectively enrolled and analyzed. Gut microbiota was analyzed using the 16S-based microbiome taxonomic profiling platform of EzBioCloud Apps and analyzing system. Results: There was a statistically significant difference among groups in diversity (P<0.05). In the comparison of phylum between cirrhosis and HCC, Proteobacteria were increased and Bacteroidetes were decreased. Firmicutes were not significantly different among the three groups. In the taxonomic profiling, relative abundance of Lactobacillus in the cirrhosis and HCC groups showed richness (P<0.05). In the biomarker analysis between cirrhosis and HCC, obiquinome Fe-S protein 3, global nitrogen regulator, Vesicle-associated membrane protein 7, toxin YoeB, peroxisome-assembly ATPase, and nitrogen oxide reductase regulator were differently expressed (P<0.001). Conclusions: Alcoholic HCC showed different expressions in the stool taxonomy and biomarker compared with that of cirrhosis and control. Therefore, new biomarkers using stool analysis for alcoholic HCC are necessary.

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“…It also enables the production of reactive oxygen species and TNF-α activation by Kupffer cells and leads to inflammation or injury to the liver. In addition, these pro-inflammatory cytokines and LPS cause the release of excess amounts of collagen and αsmooth muscle actin, which activates hepatic stellate cells and further promotes fibrosis [48][49][50][51].…”

Section: Alcohol Microbiota and Hepatocellular Carcinomamentioning

confidence: 99%

Role of Gut-Microbiota in Hepatocarcinogenesis

Gupta¹,

Youn²,

Shin³

et al. 2019

Preprint

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Hepatocellular carcinoma (HCC), one of the leading causes of death worldwide, has a causal nexus with liver injury, inflammation, and regeneration that accumulate over decades. Observations from recent studies have accounted for the involvement of the gut-liver axis in the pathophysiological mechanism responsible for HCC. The human intestine nurtures a diversified colony of microorganisms residing in the host ecosystem. The intestinal barrier is critical for conserving the normal physiology of the gut microbiome. Therefore, a rupture of this barrier or dysbiosis cause the intestinal microbiome to serve as the main source of portal-vein endotoxins such as lipopolysaccharide, in the progression of hepatic diseases. Indeed, increased bacterial translocation is a key sign of HCC. Considering the limited number of clinical studies on HCC with respect to the microbiome, we focus on the clinical as well as animal studies involving the gut microbiota with the current understandings of the mechanism by which the intestinal dysbiosis promotes hepatocarcinogenesis. Future research might offer mechanistic insights into the specific phyla targeting the leaky gut, as well as microbial dysbiosis, and their metabolites, as key pathways that drive HCC-promoting microbiome-mediated liver inflammation and fibrosis, thereby restoring the gut barrier function.

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Alcoholic hepatitis: The pivotal role of Kupffer cells

Cited by 18 publications

References 100 publications

Liver fibrosis: Pathophysiology, pathogenetic targets and clinical issues

Liver fibrosis: Pathophysiology, pathogenetic targets and clinical issues

Gut-microbiome Taxonomic Profiling as Non-invasive Biomarkers for the Early Detection of Alcoholic Hepatocellular Carcinoma

Role of Gut-Microbiota in Hepatocarcinogenesis

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