R. Balfour Sartor

TL;DR: Altered microbial composition and function in inflammatory bowel diseases result in increased immune stimulation, epithelial dysfunction, or enhanced mucosal permeability, which should lead to selective targeted interventions that correct underlying abnormalities and induce sustained and predictable therapeutic responses.

TL;DR: It is reported that Th17 cell differentiation in the lamina propria of the small intestine requires specific commensal microbiota and is inhibited by treating mice with selective antibiotics, suggesting composition of intestinal microbiota regulates the Th17:Treg balance in the LP and may thus influence intestinal immunity, tolerance, and susceptibility to inflammatory bowel diseases.

TL;DR: Gut microbes, through generation of trimethylamine N-oxide (TMAO), directly contribute to platelet hyperreactivity and enhanced thrombosis potential, revealing a previously unrecognized mechanistic link between specific dietary nutrients, gut microbes, platelet function, and thromBosis risk.

TL;DR: Current clinical trials do not fulfill evidence-based criteria for using these agents in inflammatory bowel diseases (IBD), but multiple nonrigorous studies and widespread clinical experience suggest that metronidazole and/or ciprofloxacin can treat Crohn's colitis and ileocolitis, whereas selected probiotic preparations prevent relapse of quiescent ulcerativecolitis and relapsing pouchitis.

TL;DR: Gut sterilization restricted to late stages of hepatocarcinogenesis reduced HCC, suggesting that the intestinal microbiota and TLR4 represent therapeutic targets for HCC prevention in advanced liver disease.