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Background and aimsNon-alcoholic fatty liver disease (NAFLD) is a global health burden. Risk factors for disease severity include older age, increased body mass index (BMI), diabetes, genetic variants, dietary factors and gut microbiota alterations. However, the interdependence of these factors and their individual impact on disease severity remain unknown.MethodsIn this cross-sectional study, we performed 16S gene sequencing using fecal samples, collected dietary intake, PNPLA3 gene variants and clinical and liver histology parameters in a well-described cohort of 180 NAFLD patients. Principal component analyses were used for dimensionality reduction of dietary and microbiota data. Simple and multiple stepwise ordinal regression analyses were performed.ResultsComplete data were available for 57 NAFLD patients. In the simple regression analysis, features associated with the metabolic syndrome had the highest importance regarding liver disease severity. In the multiple regression analysis, BMI was the most important factor associated with the fibrosis stage (OR per kg/m2 : 1.23, 95% CI 1.10-1.37, P

Liu, Ma and Yang for discussing our recent study about cytolysin-positive I Enterococcus faecalis (E faecalis) i in patients with non-alcoholic steatohepatitis.1 In our studies, the abundance of intestinal I E faecalis i was not associated with increased liver damage in patients with non-alcoholic fatty liver disease2 or with worse outcome in alcoholic hepatitis patients.3 However, patients with alcoholic hepatitis carrying cytolysin-positive I E faecalis i strains had a worse outcome.3 Although Drs. Liu, Ma, Yang and colleagues could show that the cell wall component lipoteichoic acid (LTA) of I E faecalis i , is able to induce inflammasome activation in vitro, it is currently unknown whether cytolysin induces inflammasome activation. The fungal peptide toxin Candidalysin activates the NLRP3 inflammasome and causes cytolysis in mononuclear phagocytes. [Extracted from the article]