Gut microbiota mediated molecular events and therapy in liver diseases

Qi, Xiaoqiang; Yang, Ming; Stenberg, Joseph; Dey, Rahul; Fogwe, Leslie; Alam, Muhammad Shawkat; Kimchi, Eric T.; Staveley-O’Carroll, Kevin F.; Li, Guangfu

doi:10.3748/wjg.v26.i48.7603

Cited by 26 publications

(19 citation statements)

References 99 publications

(60 reference statements)

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“…( 72 ) However, another investigation revealed that obese patients with NASH showed markedly higher expressions of these genes, suggesting that advanced stages of NAFLD might predispose to COVID‐19. ( 73 ) Gut microbiota and incomplete fatty acid oxidation products were also associated with NAFLD/NASH and severe COVID‐19, ( 74‐76 ) possibly by modulating host immune response. ( 77 )…”

Section: Fatty Liver and Covid‐19 Progressionmentioning

confidence: 99%

Impact of COVID‐19 in Liver Disease Progression

Martı́nez

Franco

2021

Hepatol Commun

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Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is a novel coronavirus that causes coronavirus disease 19 , which has infected millions of people worldwide in only a few months.A minority, but significant number, of infected individuals require hospitalization and intensive care. From the start of this new virus pandemic, it was apparent that obese and/or diabetic individuals had a bad prognosis for COVID-19 progression, strongly suggesting an association between liver disease and severe COVID-19. Since chronic liver disease (CLD) is associated with immune dysregulation and inflammation, it is unsurprising that CLD patients may carry a greater risk of adverse outcomes following SARS-CoV-2 infection. Initial COVID-19 data have also indicated that healthy infected individuals display abnormal liver function tests, suggesting a possible direct implication of SARS-CoV-2 in liver damage. Here we show that COVID-19 affects the liver metabolism and increases the morbidity and mortality of individuals with underlying CLD.

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Section: Fatty Liver and Covid‐19 Progressionmentioning

confidence: 99%

Impact of COVID‐19 in Liver Disease Progression

Martı́nez

Franco

2021

Hepatol Commun

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“…Firstly, gut microbial alterations were detected in patients with NAFLD. For example, in the gut of the patients with NASH or cirrhosis, there was a decrease in health-related bacteria such as Bacteroidetes and an increase of pathogenic bacteria Proteobacteria and Enterobacteriaceae specie ( 70 – 72 ); The abnormal changes in the abundance of some bacterial phyla, such as Bacteroides, Prevotella , Proteobacteria, and Firmicutes, correlate with disease severity ( 73 – 76 ).…”

Section: Gut Microbial Dysbiosis and Nafld: The Gut-liver Axismentioning

confidence: 99%

Oral and Gut Microbial Dysbiosis and Non-alcoholic Fatty Liver Disease: The Central Role of Porphyromonas gingivalis

et al. 2022

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Gut microbiota play many important roles, such as the regulation of immunity and barrier function in the intestine, and are crucial for maintaining homeostasis in living organisms. The disruption in microbiota is called dysbiosis, which has been associated with various chronic inflammatory conditions, food allergies, colorectal cancer, etc. The gut microbiota is also affected by several other factors such as diet, antibiotics and other medications, or bacterial and viral infections. Moreover, there are some reports on the oral-gut-liver axis indicating that the disruption of oral microbiota affects the intestinal biota. Non-alcoholic fatty liver disease (NAFLD) is one of the systemic diseases caused due to the dysregulation of the oral-gut-liver axis. NAFLD is the most common liver disease reported in the developed countries. It includes liver damage ranging from simple steatosis to nonalcoholic steatohepatitis (NASH), cirrhosis, and cancer. Recently, accumulating evidence supports an association between NAFLD and dysbiosis of oral and gut microbiota. Periodontopathic bacteria, especially Porphyromonas gingivalis, have been correlated with the pathogenesis and development of NAFLD based on the clinical and basic research, and immunology. P. gingivalis was detected in the liver, and lipopolysaccharide from this bacteria has been shown to be involved in the progression of NAFLD, thereby indicating a direct role of P. gingivalis in NAFLD. Moreover, P. gingivalis induces dysbiosis of gut microbiota, which promotes the progression of NAFLD, through disrupting both metabolic and immunologic pathways. Here, we review the roles of microbial dysbiosis in NAFLD. Focusing on P. gingivalis, we evaluate and summarize the most recent advances in our understanding of the relationship between oral-gut microbiome symbiosis and the pathogenesis and progression of non-alcoholic fatty liver disease, as well as discuss novel strategies targeting both P. gingivalis and microbial dysbiosis.

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“…Bile acids (BAs) play important roles in NAFLD pathogenesis by modulating hepatic lipid and glucose metabolism, consisting of primary and secondary BAs [ 26 ]. Primary BAs such as chenodeoxycholic acid (CDCA) are produced in the liver, while gut microbiota can metabolize them to secondary BAs such as deoxycholic acid (DCA) [ 9 ]. BA receptors such as nuclear Farnesoid X receptor (FXR) and the Takeda G protein-coupled receptor 5 (TGR5) are important molecules that are involved in the modulation of energy metabolism and inflammation during metabolic disorders, including NAFLD [ 27 ].…”

Section: Gut Microbiota-derived Metabolites In the Pathogenesis Nafld And Nashmentioning

confidence: 99%

“…Gut microbiota-derived molecules, such as lipopolysaccharides (LPS) and bacterial DNAs, and metabolites such as short-chain fatty acids (SCFAs), can modulate intestinal and systemic immune response [ 8 ]. Those gut microbiota-derived metabolites and components can translocate into the liver through the gut-liver axis [ 9 ], which are implicated in the initiation and progression of NAFLD. Therefore, finding the key metabolites or components-derived gut microbiota and their function in the pathogenesis of liver disease is helpful for the investigation of NAFLD therapy.…”

Section: Introductionmentioning

confidence: 99%

Diet and Gut Microbiota Interaction-Derived Metabolites and Intrahepatic Immune Response in NAFLD Development and Treatment

Yang

Khoukaz

et al. 2021

Biomedicines

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Nonalcoholic fatty liver disease (NAFLD) with pathogenesis ranging from nonalcoholic fatty liver (NAFL) to the advanced form of nonalcoholic steatohepatitis (NASH) affects about 25% of the global population. NAFLD is a chronic liver disease associated with obesity, type 2 diabetes, and metabolic syndrome, which is the most increasing factor that causes hepatocellular carcinoma (HCC). Although advanced progress has been made in exploring the pathogenesis of NAFLD and penitential therapeutic targets, no therapeutic agent has been approved by Food and Drug Administration (FDA) in the United States. Gut microbiota-derived components and metabolites play pivotal roles in shaping intrahepatic immunity during the progression of NAFLD or NASH. With the advance of techniques, such as single-cell RNA sequencing (scRNA-seq), each subtype of immune cells in the liver has been studied to explore their roles in the pathogenesis of NAFLD. In addition, new molecules involved in gut microbiota-mediated effects on NAFLD are found. Based on these findings, we first summarized the interaction of diet-gut microbiota-derived metabolites and activation of intrahepatic immunity during NAFLD development and progression. Treatment options by targeting gut microbiota and important molecular signaling pathways are then discussed. Finally, undergoing clinical trials are selected to present the potential application of treatments against NAFLD or NASH.

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Gut microbiota mediated molecular events and therapy in liver diseases

Cited by 26 publications

References 99 publications

Impact of COVID‐19 in Liver Disease Progression

Impact of COVID‐19 in Liver Disease Progression

Oral and Gut Microbial Dysbiosis and Non-alcoholic Fatty Liver Disease: The Central Role of Porphyromonas gingivalis

Diet and Gut Microbiota Interaction-Derived Metabolites and Intrahepatic Immune Response in NAFLD Development and Treatment

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