Abstract
Helicobacter pylori is a highly prevalent and harmful gastrointestinal pathogen. Antibiotic resistance and biofilm complexity have led to a decrease in the cure rate. Probiotics are considered to be an adjuvant therapy for clinical Helicobacter pylori infections. However, there is no substantial explanation for the adjuvant role of probiotics on H. pylori biofilm. In this study, the effects of probiotics in combination with amoxicillin (AMX) and clarithromycin (CLR) on H. pylori biofilms were explored in vitro for the first time. The minimum inhibitory concentration (MIC) and the fractional inhibitory concentration (FIC) for H. pylori was determined by the microbroth dilution method, and the plate counting method was used to determine the minimum biofilm removal concentration (MBEC) and survival rate for H. pylori biofilm. The biofilm structure was observed by scanning electron microscopy (SEM) and confocal laser scanning microscopy (CLSM), protein and polysaccharide contents in extracellular polymeric substances (EPS) were determined by the Bradford method and the phenol-sulfate method, respectively. The gene expression levels of cagA and vacA were evaluated by real-time qPCR. Among the ten H. pylori strains, the clinical strain 3192 showed the strongest film-forming ability, the 3192 biofilms significantly improved the resistance to AMX and CLR, and AMX and CLR showed antagonistic effects on planktonic 3192 cells. When the Lactobacillus salivarius LN12 cell-free supernatant (CFS) was in combination with AMX and CLR, the 3192 biofilm structure was destroyed to a greater extent than when separately; more biofilm biomass and protein in EPS was decreased; and the downregulation effect of the virulence gene vacA was also greater than that of single use. In this study, we suggest that the addition of LN12 to AMX and CLR may enhance the therapeutic effect of triple therapy, especially for the treatment of H. pylori biofilms.
Highlights
Lactobacillus salivarius LN12 cell-free supernatant (CFS) was in combination with AMX and CLR, the 3192 biofilm structure was destroyed to a greater extent than when separately; more biofilm biomass and protein in extracellular polymeric substances (EPS) was decreased; and the downregulation effect of the virulence gene vacA was greater than that of single use
Twelve percent of all strains were resistant to amoxicillin, 50% were resistant to clarithromycin, 50% were resistant to levofloxacin, 87.5% were resistant to metronidazole, and 0% were resistant to tetracycline
Due to the severely increasing global antibiotic resistance, in areas where the resistance to clarithromycin is higher than 20%, the efficacy of triple therapy containing amoxicillin and clarithromycin has been lower than 80% [33]
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.Licensee MDPI, Basel, Switzerland.Attribution (CC BY) license (https://creativecommons.org/licenses/by/ 4.0/).Helicobacter pylori (H. pylori) is a spiral-shaped Gram-negative pathogen that colonizes the stomach in approximately half of the world’s population. It can spread from person to person and is closely related to peptic ulcer disease, atrophic gastritis, gastric adenocarcinoma, and MALT. Although H. pylori prevalence varies from country to country, the infection rate in developing countries is relatively high (80–90%). It was designated as a class I carcinogen by the World Health Organization (WHO) in 1994 [1,2]. The Maastricht
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