[18] Another successful example of probiotics from mouse studies is a report that the Lactobacillus casei strain Shirota is able to protect mice against SCH 900776 the onset of NAFLD by way of an attenuation of the TLR4-signaling cascade in the liver and

an increased peroxisome proliferator-activated receptor (PPAR)-γ activity.[73] Another interesting candidate for the probiotic management of liver disease is Bifidobacterium pseudocatenulatum CECT 7765; a recent study demonstrates that the administration of this probiotic bacteria improves various metabolic alterations in the HFD-fed mouse model, and is interestingly able to reduce liver steatosis.[74] Of note, the changes in gut microbiota composition induced by polyunsaturated fatty acids-depletion and prebiotics administration (fructo-oligosaccharides) is able Selleck JNK inhibitor to modulate hepatic steatosis by changing gene expression in the liver, suggesting that a prebiotic approach could be conceivable in the management of liver disease.[75] Probiotics may also be promising way to restore the “leaky gut” state observed in numerous patients with liver

disease; Escherichia coli strain Nissle 1917 is able to restore normal mucosal permeability in the murine dextran sulfate sodium (DSS)-induced colitis model, as well as induce up-regulation of zonula occludens 1 expression in vitro.[76] Similarly, probiotic mixture VSL#3 is able to prevent the increased intestinal permeability induced by a DSS treatment, phenomena associated with a prevention of decreased expression and redistribution of the tight junction proteins occludin, zonula occludens-1, and claudin-1, -3, -4, and -5 normally observed in DSS-treated mice.[77] Antibiotics, by themselves, seem unlikely to be an effective means of promoting a healthful host-microbiota relationship, but could be part of approaches to transplant microbiotas. While, at present, the beneficial effects of microbiota transplant are only proven to prevent recurrent Clostridium

difficile colitis,[78] a recent study found that microbiota transplant ameliorated insulin resistance,[79] suggesting that the approach might be broadly applicable to various aspects of metabolic syndrome, click here including NAFLD. Thus, while further studies are warranted, it is the opinion of the authors that manipulation of the gut microbiota will ultimately be a helpful means of treating and/or preventing liver disease. It has long been appreciated that environmental factors, including diet and infection, are major determinants of liver disease. Herein we reviewed evidence supporting the more recently appreciated concept that another important environmental factor is the large microbial biomass living in the intestine. Being close the liver, the gut microbiota can influence liver phenotype in a number of ways.