Microbiota and the liver

Shen, Ting-Chin David; Pyrsopoulos, Nikolaos; Rustgi, Vinod K.

doi:10.1002/lt.25008

Cited by 35 publications

(25 citation statements)

References 96 publications

(202 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The main fermentation products are short chain fatty acids (SCFAs), acetate, propionate, and butyrate [5]. Butyrate acts as an energy source for the colonic epithelium, whereas acetate and propionate serve as substrates for lipogenesis and gluconeogenesis [6,7]. The bacterial short chain fatty acids (SCFAs) thus work as additional sources of energy, constituting 3%-9% of our daily caloric intake [8].…”

Section: Short Chain Fatty Acidsmentioning

confidence: 99%

“…The rest escapes the EHC and becomes substrate for microbial transformation in the right colon [11]. Conjugated primary bile acids (CDCA and CA) undergo microbial modifications (e.g., deconjugation, dehydroxylation, and hydrogenation) to form secondary bile acids lithocholic acid (LCA) and deoxycholic acid (DCA), respectively [7]. The colonic 7α-dehydroxylating bacteria (e.g., Lachonospiraceae, Ruminococcaceae, and Blautia) play a key role in this conversion.…”

Section: Bile Acidsmentioning

confidence: 99%

See 1 more Smart Citation

Role of Gut Dysbiosis in Liver Diseases: What Have We Learned So Far?

Fukui

2019

Diseases

View full text Add to dashboard Cite

Accumulating evidence supports that gut dysbiosis may relate to various liver diseases. Alcoholics with high intestinal permeability had a decrease in the abundance of Ruminnococcus. Intestinal dysmotility, increased gastric pH, and altered immune responses in addition to environmental and genetic factors are likely to cause alcohol-associated gut microbial changes. Alcohol-induced dysbiosis may be associated with gut barrier dysfunction, as microbiota and their products modulate barrier function by affecting epithelial pro-inflammatory responses and mucosal repair functions. High levels of plasma endotoxin are detected in alcoholics, in moderate fatty liver to advanced cirrhosis. Decreased abundance of Faecalibacterium prausnitzii, an anti-inflammatory commensal, stimulating IL-10 secretion and inhibiting IL-12 and interferon-γ expression. Proteobacteria, Enterobacteriaceae, and Escherichia were reported to be increased in NAFLD (nonalcoholic fatty liver disease) patients. Increased abundance of fecal Escherichia to elevated blood alcohol levels in these patients and gut microbiota enriched in alcohol-producing bacteria produce more alcohol (alcohol hypothesis). Some undetermined pathological sequences related to gut dysbiosis may facilitate energy-producing and proinflammatory conditions for the progression of NAFLD. A shortage of autochthonous non-pathogenic bacteria and an overgrowth of potentially pathogenic bacteria are common findings in cirrhotic patients. The ratio of the amounts of beneficial autochthonous taxa (Lachnospiraceae + Ruminococaceae + Veillonellaceae + Clostridiales Incertae Sedis XIV) to those of potentially pathogenic taxa (Enterobacteriaceae + Bacteroidaceae) was low in those with early death and organ failure. Cirrhotic patients with decreased microbial diversity before liver transplantation were more likely to develop post-transplant infections and cognitive impairment related to residual dysbiosis. Patients with PSC had marked reduction of bacterial diversity. Enterococcus and Lactobacillus were increased in PSC patients (without liver cirrhosis.) Treatment-naive PBC patients were associated with altered composition and function of gut microbiota, as well as a lower level of diversity. As serum anti-gp210 antibody has been considered as an index of disease progression, relatively lower species richness and lower abundance of Faecalibacterium spp. in gp210-positive patients are interesting. The dysbiosis-induced altered bacterial metabolites such as a hepatocarcinogenesis promotor DCA, together with a leaky gut and bacterial translocation. Gut protective Akkermansia and butyrate-producing genera were decreased, while genera producing-lipopolysaccharide were increased in early hepatocellular carcinoma (HCC) patients.

show abstract

Section: Short Chain Fatty Acidsmentioning

confidence: 99%

Section: Bile Acidsmentioning

confidence: 99%

Role of Gut Dysbiosis in Liver Diseases: What Have We Learned So Far?

Fukui

2019

Diseases

View full text Add to dashboard Cite

show abstract

“…Under pathological conditions when the intestinal barrier is impaired with an increased translocation of microbial products, an inflammatory process is initiated leading to liver damage impairing hepatocyte function and detoxification potential, which may lead to inflammatory liver diseases. Lipopolysaccharides (LPS) trigger toll-like receptor 4 (TLR4) expressed by Kupffer and hepatic stellate cells to activate transforming growth factor β signaling that leads to the development of hepatic fibrosis and eventually cirrhosis [ 36 ]. In end-stage liver disease, microbial products that cannot be cleared by the liver get into the systemic circulation, activating immune cells and leading to damage of distant organs.…”

Section: Discussionmentioning

confidence: 99%

“…A dysbiosis with translocation of microbes and of microbial products when this barrier is disrupted may cause or worsen various hepatic diseases through this interdependence of gut and liver. Dysbiosis has been associated with many chronic liver conditions such as nonalcoholic fatty liver disease (NAFLD) or nonalcoholic steato-hepatitis (NASH), alcoholic liver disease (ALD), as well as cirrhosis and its complications like hepatic malignancy [ 36 ].…”

Section: Introductionmentioning

confidence: 99%

Effects of both Pro- and Synbiotics in Liver Surgery and Transplantation with Special Focus on the Gut–Liver Axis—A Systematic Review and Meta-Analysis

2020

View full text Add to dashboard Cite

The gut-liver axis is of upmost importance for the development of infections after surgery. Further bacterial translocation due to surgery-related dysbiosis is associated with limited detoxification function of the liver compromising outcome of surgical therapy. After liver surgery, about 30% of patients develop a bacterial infection, with the risk of bacteremia or even sepsis-associated liver failure and mortality in >40%. The potential benefit of pro-/synbiotics given before surgery is still under debate. Thus, a systematic literature search on trials comparing patients with or without supplementation and outcome after liver resection or transplantation was performed. Our search strategy revealed 12 relevant studies on perioperative administration of pro-/synbiotics in liver surgery. The pro-/synbiotic combinations and concentrations as well as administration timeframes differed between studies. Five studies were performed in liver transplantation and 7 in liver resection. All studies but one reported lower infection rates (pooled RR: 0.46, 95% CI: 0.31–0.67) with pro-/synbiotics. Liver function was assessed after LT/LR in 3 and 5 studies, respectively. Pro-/synbiotics improved function in 1/3 and 2/5 studies, respectively. Concluding, perioperative pro-/synbiotics clearly reduce infection after liver surgery. However, standard protocols with both well-defined probiotic strain preparations and administration timeframes are pending.

show abstract

“…(25,31,32) The presence of dysbiosis in ESLD has been studied and reviewed in great detail. (18,(33)(34)(35)(36)(37) Specifically, the microbial composition in patients with ESLD tends to have increased pathogenic bacteria from the Enterobacteriaceae and decreased commensal organisms from the Firmicutes phylum. The reduced enterohepatic circulation of BAs, impaired gut motility, and small intestinal bacterial overgrowth in ESLD have been implicated in the development of these disruptions in the microbiome.…”

Section: The Gut Microbiota and Liver Diseasementioning

confidence: 99%

The Microbiome and Hepatocellular Carcinoma

2020

View full text Add to dashboard Cite

The human microbiome is a vast and complex system encompassing all of the microbes and their genes that occupy the environmentally exposed surfaces of the human body. The gut microbiota and its associated microbiome play an integral role in mammalian metabolism and immune tolerance as well as in immunocompetence. Disruptions in the human gut microbiome are associated with a cycle of hepatocyte injury and regeneration characteristic of chronic liver disease. The persistence of this inflammation has been shown to induce the accumulation of genetic and epigenetic changes leading to hepatocellular carcinoma (HCC). Therefore, the importance and prognostic influence of the gut microbiome on hepatocarcinogenesis has been increasingly studied in recent years. This review discusses the mechanisms by which imbalances in the gut microbiome disturb the gut‐liver axis to impact hepatocarcinogenesis, including disruption of the intestinal barrier, changes in bile acid metabolism, and reduction in tumor‐suppressing microRNA. Furthermore, this review summarizes recent advances in potential microbiome‐based therapeutic opportunities in HCC.

show abstract

Microbiota and the liver

Cited by 35 publications

References 96 publications

Role of Gut Dysbiosis in Liver Diseases: What Have We Learned So Far?

Role of Gut Dysbiosis in Liver Diseases: What Have We Learned So Far?

Effects of both Pro- and Synbiotics in Liver Surgery and Transplantation with Special Focus on the Gut–Liver Axis—A Systematic Review and Meta-Analysis

The Microbiome and Hepatocellular Carcinoma

Contact Info

Product

Resources

About