Cytolysin‐positive <i>Enterococcus faecalis</i> is not increased in patients with non‐alcoholic steatohepatitis

Lang, Sonja; Demir, Münevver; Duan, Yi; Martin, Anna; Schnabl, Bernd

doi:10.1111/liv.14377

Cited by 30 publications

(22 citation statements)

References 8 publications

(17 reference statements)

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“…31 The presence of cytolysin-positive (cytolytic) E. faecalis correlates with liver disease severity and mortality in patients with alcoholic hepatitis, 31 but no correlation was found in patients with non-alcoholic fatty liver disease. 32 Bacterial infections are a serious complication of cirrhosis, as they can lead to decompensation, multiple organ failure, and/or death. Because bacterial translocation from the gut lumen to extraintestinal sites causes infections, prevention of infections is http://www.e-cmh.org https://doi.org/10.3350/cmh.2020.0086 mostly based on the use of orally administered, poorly absorbed antibiotics (known as selective intestinal decontamination).…”

Section: Intestinal Dysbiosismentioning

confidence: 99%

From intestinal dysbiosis to alcohol-associated liver disease

Mendes

Schnabl

2020

Clin Mol Hepatol

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Alcohol-associated intestinal dysbiosis and bacterial overgrowth can lead to a dysregulation of tryptophan metabolism and lower production of indoles. Several of these indole derivatives are aryl hydrocarbon receptor ligands that, in turn, are involved in antimicrobial defense via induction of interleukin-22 (IL-22). IL-22 increases the expression of intestinal regenerating islet-derived 3 (Reg3) lectins, which maintain low bacterial colonization of the inner mucus layer and reduce bacterial translocation to the liver. Chronic alcohol consumption is associated with reduced intestinal expression of Reg3β and Reg3γ, increased numbers of mucosa-associated bacteria and bacterial translocation. Translocated microbial products and viable bacteria reach the liver and activate the innate immune system. Release of inflammatory molecules promotes inflammation, contributes to hepatocyte death and results in a fibrotic response. This review summarizes the mechanisms by which chronic alcohol intake changes the gut microbiota and contributes to alcohol-associated liver disease by changing microbial-derived metabolites.

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Section: Intestinal Dysbiosismentioning

confidence: 99%

From intestinal dysbiosis to alcohol-associated liver disease

Mendes

Schnabl

2020

Clin Mol Hepatol

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“…Thus, NAFLD patients received the same overall lifestyle recommendations as indicated in the current European guideline 20 . Further exclusion criteria for NAFLD patients were ongoing successful lifestyle modifications defined as more than 5% loss of body weight within the last three months prior to enrollment or current or prior participation in an interventional non-alcoholic steatohepatitis (NASH) study 21 .…”

Section: Methodsmentioning

confidence: 99%

“…The NAFLD activity score was obtained for each biopsy. This score is defined as the unweighted sum of the scores for steatosis, (0-3), lobular inflammation (0-3), and ballooning (0-2); thus ranging from 0 to 8 21,22 .…”

Section: Methodsmentioning

confidence: 99%

“…nodular hepatic contour, changes in volume distribution indicating portal hypertension in the absence of portal vein thrombosis, secondary phenomena of portal hypertension such as splenomegaly, enlarged caudate lobe and left lobe lateral segment, regenerative nodules) together with clinical and laboratory signs of portal hypertension/cirrhosis (e.g. low platelets, albumin and prothrombin time, esophageal varices) 21,23 .…”

Section: Methodsmentioning

confidence: 99%

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Prediction of advanced fibrosis in non-alcoholic fatty liver disease using gut microbiota-based approaches compared with simple non-invasive tools

Lang

Farowski

Martin

et al. 2020

Sci Rep

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Liver fibrosis is the major determinant of liver related complications in patients with non-alcoholic fatty liver disease (NAFLD). A gut microbiota signature has been explored to predict advanced fibrosis in NAFLD patients. The aim of this study was to validate and compare the diagnostic performance of gut microbiota-based approaches to simple non-invasive tools for the prediction of advanced fibrosis in NAFLD. 16S rRNA gene sequencing was performed in a cohort of 83 biopsy-proven NAFLD patients and 13 patients with non-invasively diagnosed NAFLD-cirrhosis. Random Forest models based on clinical data and sequencing results were compared with transient elastography, the NAFLD fibrosis score (NFS) and FIB-4 index. A Random Forest model containing clinical features and bacterial taxa achieved an area under the curve (AUC) of 0.87 which was only marginally superior to a model without microbiota features (AUC 0.85). The model that aimed to validate a published algorithm achieved an AUC of 0.71. AUC's for NFS and FIB-4 index were 0.86 and 0.85. Transient elastography performed best with an AUC of 0.93. Gut microbiota signatures might help to predict advanced fibrosis in NAFLD. However, transient elastography achieved the best diagnostic performance for the detection of NAFLD patients at risk for disease progression. Non-alcoholic fatty liver disease (NAFLD) is a global health issue with growing incidence 1. Some patients with simple steatosis develop liver fibrosis which can lead to cirrhosis, hepatocellular carcinoma, liver transplantation and death 2,3. The presence of liver fibrosis is the major determinant of future liver related complications 4,5. Liver biopsy, an invasive procedure with an inherent risk of complications remains the gold-standard for disease grading and staging.

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“…The study cohort has been described previously. (19) A total of 61 patients with NAFLD with available liver biopsy results and dietary records were included in the analysis, with the aim of detecting associations between histological disease activity and dietary nutrient intake. A total of 99 patients with NAFLD with fecal samples and dietary record were included in the analysis that aimed to investigate associations of nutrients with different abundances in the gut microbiota, whereas 59 patients of the biopsy-proven cohort were overlapping and included in the microbiota analysis.…”

Section: High Protein Intake Is Associated With Histological Disease mentioning

confidence: 99%

High Protein Intake Is Associated With Histological Disease Activity in Patients With NAFLD

Lang

Martin²,

Farowski

et al. 2020

Hepatol Commun

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Overconsumption of carbohydrates and lipids are well known to cause nonalcoholic fatty liver disease (NAFLD), while the role of nutritional protein intake is less clear. In Western diet, meat and other animal products are the main protein source, with varying concentrations of specific amino acids. Whether the amount or composition of protein intake is associated with a higher risk for disease severity has not yet been examined. In this study, we investigated associations of dietary components with histological disease activity by analyzing detailed 14-day food records in a cohort of 61 patients with biopsy-proven NAFLD. Furthermore, we used 16S ribosomal RNA gene sequencing to detect associations with different abundances of the gut microbiota with dietary patterns. Patients with definite nonalcoholic steatohepatitis (NAFLD activity score of 5-8 on liver biopsy) had a significantly higher daily relative intake of protein compared with patients with a NAFLD activity score of 0-4 (18.0% vs. 15.8% of daily protein-based calories, P = 0.018). After adjustment for several potentially confounding factors, a higher protein intake (≥17.3% of daily protein-based calories) remained associated with definite nonalcoholic steatohepatitis, with an odds ratio of 5.09 (95% confidence interval 1.22-21.25, P = 0.026). This association was driven primarily by serine, glycine, arginine, proline, phenylalanine, and methionine. A higher protein intake correlated with a lower Bacteroides abundance and an altered abundance of several other bacterial taxa. Conclusion: A high protein intake was independently associated with more active and severe histological disease activity in patients with NAFLD. Further studies are needed to investigate the potential harmful role of dietary amino acids on NAFLD, with special attention to meat as their major source. (Hepatology Communications 2020;4:681-695).

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Cytolysin‐positive Enterococcus faecalis is not increased in patients with non‐alcoholic steatohepatitis

Cited by 30 publications

References 8 publications

From intestinal dysbiosis to alcohol-associated liver disease

From intestinal dysbiosis to alcohol-associated liver disease

Prediction of advanced fibrosis in non-alcoholic fatty liver disease using gut microbiota-based approaches compared with simple non-invasive tools

High Protein Intake Is Associated With Histological Disease Activity in Patients With NAFLD

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