No abstract

Background/Aim The interactions between the gut and liver have been described in the progression of non-alcoholic steatohepatitis (NASH). The aim of this study was to develop an experimental nutritional model of NASH simulating metabolic changes occurring in humans. Materials and Methods Adult male Sprague Dawley rats were randomized into two groups: controls (standard diet) and intervention (high-fat and choline-deficient diet) for 16 weeks, each experimental group with 10 animals. Biochemical analysis, hepatic lipid content, microRNAs, inflammatory, gut permeability markers and gut microbiota were measured. Results Animals in the intervention group showed significantly higher delta Lee index ( p =0.017), abdominal circumference ( p <0.001), abdominal adipose tissue ( p <0.001) and fresh liver weight ( p <0.001), as well as higher serum levels of alanine aminotransferase ( p =0.010), glucose ( p =0.013), total cholesterol ( p =0.033), LDL cholesterol ( p =0.011), and triglycerides ( p =0.011), and lower HDL cholesterol ( p =0.006) compared to the control group. Higher TLR4 ( p =0.041), TLR9 ( p =0.033), MyD88 ( p =0.001), Casp1 ( p <0.001), NLPR3 ( p =0.019), liver inflammation index interleukin (IL)-1β/IL10 ( p <0.001), IL6/IL10 ( p =0.002) and TNFα/IL10 ( p =0.001) were observed in the intervention group, and also lower permeability markers Ocln ( p =0.003) and F11r ( p =0.041). Gene expression of miR-122 increased ( p =0.041) and miR-145 ( p =0.010) decreased in the intervention group. Liver steatosis, inflammation and fibrosis, along with collagen fiber deposition increment ( p <0.001), were seen in the intervention group. Regarding gut microbiota, Bray-Curtis dissimilarity index and number of operational taxonomic units were significantly different ( p <0.001) between the groups. Composition of the gut microbiota showed a significant correlation with histopathological score of NAFLD (r=0.694) and index IL-1β/IL-10 (r=0.522). Conclusion This experimental model mimicking human NASH demonstrated gut and liver interaction, with gut microbiota and intestinal permeability changes occurring in parallel with systemic and liver inflammation, miRNAs regulation and liver tissue damage.

Introduction: Helicobacter pylori is a bacteria which infects half the world population and is an important cause of gastric cancer. The eradication therapy is not always effective because resistance to antimicrobials may occur. The aim of this study was to determine the susceptibility profile of H. pylori to amoxicillin, clarithromycin and ciprofloxacin in the population of Southern Brazil. Material and methods: Fifty four samples of H. pylori were evaluated. The antibiotics susceptibility was determined according to the guidelines of the British Society for Antimicrobial Chemotherapy and the Comité de l'Antibiogramme de la Société Française de Microbiologie. Results: Six (11.1%) H. pylori isolates were resistant to clarithromycin, one (1.9%) to amoxicillin and three (5.5%) to ciprofloxacin. These indices of resistance are considered satisfactory and show that all of these antibiotics can be used in the empirical therapy. Conclusion: The antibiotics amoxicillin and clarithromycin are still a good option for first line anti-H. pylori treatment in the population of Southern Brazil.