Background: The aim of this study was to assess the disk diffusion technique against E‐test as a routine antibiotic susceptibility testing method for Helicobacter pylori.Materials and methods: Susceptibilities of 301 H pylori clinical isolates were simultaneously profiled by E‐test and disk diffusion method for levofloxacin (5‐μg disk), clarithromycin (15‐μg disk), metronidazole (5‐μg disk), amoxicillin (10‐μg disk), and tetracycline (30‐μg disk). Furazolidone susceptibility was evaluated using a 100‐μg disk only. The correlation between MICs by E‐test and inhibition zone diameters by disk diffusion was assessed by linear regression analysis.Results: Correlation between inhibition zone diameters and MICs was found for levofloxacin (r = −.932), clarithromycin (r = −.894), and to a minor extent metronidazole (r = −.820). Using the linear regression analysis, the inhibition zone diameter breakpoints were calculated to be 29 mm for levofloxacin, 41 mm for clarithromycin, and 15 mm for metronidazole corresponding to the EUCAST‐recommended MIC breakpoints. The susceptibility agreement between E‐test and disk diffusion for levofloxacin, clarithromycin, and metronidazole was 98.6%, 96.0%, and 96.7%, respectively. The inhibition zone diameters recorded for the amoxicillin, tetracycline, and furazolidone were large (approximately 60 mm in mean), and a poor correlation was found between inhibition zone diameters and MICs for amoxicillin (r = −.594) and tetracycline (r = −.490).Conclusions: The disk diffusion can be used as a routine H pylori susceptibility testing method for levofloxacin, clarithromycin, and metronidazole in clinical practice under the described technical conditions. The use of disk diffusion for amoxicillin, tetracycline, and furazolidone susceptibility testing needs to be further studied.

Helicobacter pylori infection is an infectious disease and thus the eradication treatment should be guided by susceptibility testing. This study aimed to assess the applicability of broth microdilution as a routine susceptibility testing method for H. pylori. Susceptibility profiles of clarithromycin (CLR) and levofloxacin (LEV) resistance in 76 clinical H. pylori isolates were simultaneously assessed using agar dilution and broth microdilution methods. The correlation between the minimum inhibitory concentrations (MICs) obtained by the 2 methods was assessed by means of linear regression analysis. The correlation between the MICs determined by broth microdilution method and agar dilution method was good for both CLR (r = 0.966) and LEV (r = 0.959). The susceptibility agreement between the 2 methods was 100% for CLR and 96.1% for LEV. Using the broth microdilution method, the false resistance was found in 3.9% (3 of 76) strains for LEV susceptibility testing. No false susceptibility was found for either CLR or LEV, and no false resistance was found for susceptibility testing of CLR. The broth microdilution method is suitable for routine susceptibility testing of clinical H. pylori isolates.

Helicobacter pylori infection is an infectious disease. Given the alarmingly high antibiotic resistance in H. pylori, gastroenterologists should change the empiric H. pylori treatment paradigm to an antimicrobial susceptibility testing-guided precision treatment. Antimicrobial stewardship programs for H. pylori should be implemented locally, regionally, and nationally to monitor the antibiotic resistance pattern.

Ectopic fat deposition in the liver, known as non-alcoholic fatty liver disease (NAFLD), affects up to 30% of the worldwide population. miRNA-122, the most abundant liver-specific miRNA, protects hepatic steatosis and inhibits cholesterol and fatty acid synthesis in NAFLD. Previously, we have shown that compared with its expression in healthy controls, miRNA-122 decreased in the liver tissue but gradually increased in the serum of patients with non-alcoholic fatty liver disease and non-alcoholic steatohepatitis, suggesting that miRNA-122 could have been transported to the serum. Here, we aimed to confirm and unravel the mechanism of transportation of miRNA-122 to extra-hepatocytes. Our findings showed a decrease in the intra-hepatocyte miRNA-122 and an increase in the extra-hepatocyte (medium level) miRNA-122, suggesting the miRNA-122 “escaped” from the intra-hepatocyte due to an increased extra-hepatocyte excretion. Using bioinformatics tools, we showed that miRNA-122 binds to circPI4KB, which was further validated by an RNA pull-down and luciferase reporter assay. The levels of circPI4KB in intra- and extra-hepatocytes corresponded to that of miRNA-122, and the overexpression of circPI4KB increased the miRNA-122 in extra-hepatocytes, consequently accomplishing a decreased protective role of miRNA-122 in inhibiting the lipid deposition. The present study provides a new explanation for the pathogenesis of the hepatic lipid deposition in NAFLD.