The effect of previous eradication failure on antibiotic resistance of Helicobacter pylori: A retrospective study over 8 years in Beijing.

BACKGROUND: Antibiotic resistance is the main cause of Helicobacter pylori (H. pylori) treatment failure. This study aimed to explore the characteristics of antibiotic resistance of H. pylori isolates in Beijing in the last 8 years and to estimate the impact of previous eradication failure on resistance patterns. MATERIALS AND METHODS: This retrospective study included data from a single center in Beijing from 2013 to 2020. Antibiotic susceptibility of 365 clinical H. pylori isolates was tested for amoxicillin, clarithromycin, metronidazole, levofloxacin, moxifloxacin, and tetracycline. The characteristics of the included patients and their previous eradication history were collected. Primary and secondary resistance rates of H. pylori to the six antibiotics and the impact of previous eradication failure on antibiotic resistance patterns were analyzed. RESULTS: The overall primary resistance rates of amoxicillin, clarithromycin, metronidazole, levofloxacin, moxifloxacin, and tetracycline were 0.7%, 55.2%, 68.0%, 49.7%, 64.5%, and 0%, with no significant increase during the observed period; while the secondary resistance rates were 3.2%, 96.7%, 90.7%, 93.1%, 80.0%, and 0%, respectively. The secondary resistance rate of clarithromycin (p < .001), metronidazole (p = .001), and levofloxacin (p < .001) significantly increased to 100% as the number of previous eradication therapies increased and exhibited a linear association. For strains naive to eradication, only 6.8% were susceptible to all the antibiotics, while 32.4% were single resistant, and 60.8% dual or multiple resistant. Clarithromycin+metronidazole+fluoroquinolone multiple resistance was the predominant pattern (0 course: 21.6%, 1 course: 37.5%, 2 courses: 56.1%, ≥3 courses: 71.1%; p < .001) for patients with treatment failure. The prevalence of dual or multiple-resistance patterns increased significantly as the number of previous therapies increased. CONCLUSIONS: The prevalence of primary and secondary resistance rates of clarithromycin, metronidazole, moxifloxacin, and levofloxacin were high in Beijing. Multiple-resistance patterns were common after treatment failure. Resistance rates of amoxicillin and tetracycline remained low and stable.

Effects of combined high pressure and enzymatic treatments on physicochemical and antioxidant properties of peanut proteins.

Isolated peanut protein (PPI) dispersions were pretreated by high pressure at 100, 300, and 500 MPa prior to enzymatic hydrolysis with alkaline protease (Alcalase). The degree of hydrolysis (DH) was determined by the pH-stat method, the hydrolysates profiles were analyzed by high-performance liquid chromatography (HPLC), the molecular weight distribution (MWD) was analyzed by gel filtration chromatogram (GFC), and content of SH/S-S and antioxidant activity of hydrolysates were evaluated. Results showed that HP pretreatment improved effectively the enzymatic hydrolysis of PPI, with an effective sequence of 300 > 100 > 500 MPa. However, no significant differences were observed in the peak pattern of HPLC profiles, but the peak times were earlier in HPLC profiles of the HP-treated protein. GFC analysis showed that more peptide fractions with low molecular weight appeared in the hydrolysates of the HP-treated PPI with increasing pressure. Moreover, the level of free SH of hydrolysates of the HP-treated PPI was relatively higher than non-HP-treated PPI. The hydrolysates of the HP-treated PPI exerted higher antioxidant activity (reducing power and DPPH radical scavenging) than the hydrolysates of non-HP-treated PPI. The results indicated that high pressure treatment affected the enzymatic hydrolysis of peanut protein and some protein structure properties and improved antioxidant activity of PPI hydrolysates.

Role of Porphyromonas gingivalis outer membrane vesicles in oral mucosal transmission of HIV.

The association between mucosal microbiota and HIV-1 infection has garnered great attention in the field of HIV-1 research. Previously, we reported a receptor-independent HIV-1 entry into epithelial cells mediated by a Gram-negative invasive bacterium, Porphyromonas gingivalis. Here, we present evidence showing that P. gingivalis outer membrane vesicles (OMVs) promote mucosal transmission of HIV-1. We demonstrated, using the Dynabeads technology, a specific interaction between HIV-1 and P. gingivalis OMVs which led to an OMV-dependent viral entry into oral epithelial cells. HIV-1 was detected in human oral keratinocytes (HOKs) after a 20 minute exposure to the HIV-vesicle complexes. After entry, most of the complexes appeared to dissociate, HIV-1 was reverse-transcribed, and viral DNA was integrated into the genome of HOKs. Meanwhile, some of the complexes exited the original host and re-entered neighboring HOKs and permissive cells of HIV-1. Moreover, P. gingivalis vesicles enhanced HIV-1 infection of MT4 cells at low infecting doses that are not able to establish an efficient infection alone. These findings suggest that invasive bacteria and their OMVs with ability to interact with HIV-1 may serve as a vehicle to translocate HIV through the mucosa, establish mucosal transmission of HIV-1, and enhance HIV-1 infectivity.