OBJECTIVES: Helicobacter pylori resistance to antibiotics is the main factor for therapy failure, while other features remain largely unknown. The aims of this study are to investigate the relationship of antibiotic resistance and in vitro internalization activity between cure and failure isolates and to determine whether failures are associated with persistence of the same predominant strain. METHODS: Fifty-three isolates from forty-seven patients (cure group, n = 31; failure group, n = 16) receiving one of two lansoprazole-based therapies before and/or after therapy were investigated. Antibiotic susceptibility was determined by Etest. Genotyping was determined by cagA, babA, vacA and RAPD analyses. Target cells of internalization assay were AGS cells. RESULTS: Five of six paired pre- and post-treatment isolates had the same predominant genetic profiles and exhibited similarly high internalization activities. The A2143G point mutation of the 23S rRNA gene conferred clarithromycin resistance. Moreover, increased antibiotic resistance after therapy was found for these five cases. Pre-treatment isolates from the failure group (n = 11) had higher level of internalization activity than those from the cure group (n = 31) (P = 0.00005). Antibiotic-resistant strains were significantly associated with higher internalization activity than were susceptible strains (metronidazole, P < 0.005; clarithromycin, P < 0.005). CONCLUSIONS: Our results suggest that resistant H. pylori strains are associated with antibiotic resistance and superior internalization activity, protecting them against antibiotic treatment.
OBJECTIVES:Helicobacter pylori resistance to antibiotics is the main factor for therapy failure, while other features remain largely unknown. The aims of this study are to investigate the relationship of antibiotic resistance and in vitro internalization activity between cure and failure isolates and to determine whether failures are associated with persistence of the same predominant strain. METHODS: Fifty-three isolates from forty-seven patients (cure group, n = 31; failure group, n = 16) receiving one of two lansoprazole-based therapies before and/or after therapy were investigated. Antibiotic susceptibility was determined by Etest. Genotyping was determined by cagA, babA, vacA and RAPD analyses. Target cells of internalization assay were AGS cells. RESULTS: Five of six paired pre- and post-treatment isolates had the same predominant genetic profiles and exhibited similarly high internalization activities. The A2143G point mutation of the 23S rRNA gene conferred clarithromycin resistance. Moreover, increased antibiotic resistance after therapy was found for these five cases. Pre-treatment isolates from the failure group (n = 11) had higher level of internalization activity than those from the cure group (n = 31) (P = 0.00005). Antibiotic-resistant strains were significantly associated with higher internalization activity than were susceptible strains (metronidazole, P < 0.005; clarithromycin, P < 0.005). CONCLUSIONS: Our results suggest that resistant H. pylori strains are associated with antibiotic resistance and superior internalization activity, protecting them against antibiotic treatment.