Abstract
Helicobacter pylori is a gastrointestinal pathogen with a high infection rate. Probiotics are clinically used as an adjuvant to improve the cure rate and reduce the side effects of antibiotic treatment for H. pylori. This study is the first to explore the effects of a cell-free supernatant of high- or low-dose Lactobacillus salivarius LN12 combined with amoxicillin (AMX) and clarithromycin (CLR) on H. pylori 3192 biofilms in terms of the biofilm biomass, survival rates, biofilm structure, and transcriptome. The results showed that the combination of the CFS of high-dose LN12 with AMX and CLR had stronger effects on the biofilm biomass, survival rate, and structure of H. pylori 3192 biofilms. H. pylori 3192 biofilms may increase the expression of NADH-related genes and downregulate flagellar assembly and quorum sensing-related receptor genes to deal with the stronger stress effects of high-dose LN12 with AMX and CLR. In conclusion, the biofilm biomass, survival rate, structure, and transcriptome results showed that the combination of LN12 CFS with AMX and CLR had dose effects. We recommend that compared with low doses, high doses of L. salivarus LN12 combined with AMX and CLR may be more effective for H. pylori biofilm than low doses.
Highlights
As microaerobic Gram-negative bacteria, Helicobacter pylori (H. pylori) can colonize the human stomach through the oral cavity and is closely linked to chronic gastritis, peptic ulcers, gastric mucosa-associated lymphoid tissue lymphoma, and other gastric disorders [1,2]
H. pylori 3192 biofilm was treated with cell-free supernatant (CFS) of high- and low-dose L. salivarus LN12 combined with AMX and CLR for the first time in vitro
Compared with that of low-dose L. salivarus LN12, the CFS of high-dose L. salivarus LN12 combined with AMX and CLR had more significant destructive effects on the H. pylori 3192 biofilm biomass, survival rate and biofilm structure
Summary
As microaerobic Gram-negative bacteria, Helicobacter pylori (H. pylori) can colonize the human stomach through the oral cavity and is closely linked to chronic gastritis, peptic ulcers, gastric mucosa-associated lymphoid tissue lymphoma, and other gastric disorders [1,2]. The global infection rate of H. pylori is more than 50% and affected by geographical and economic conditions, the infection rate in developing countries is higher than that in developed countries, and H. pylori was listed as a group I carcinogen by the. The spirochete shape and flagellum structure of H. pylori help it move in the harsh low-pH environment of the stomach, and a variety of adhesion proteins and urease secreted by H. pylori facilitate its effective colonization. H. pylori can form biofilm structures in vivo and in vitro, which are composed of protein, mannan, LPS-related structures, extracellular. Biofilms can enhance resistance to antibiotics, improve the persistence and survival rate in the host, and reduce the success rate of treatment [5]. The regulatory process of H. pylori biofilm formation has not been fully explained, and in particular, transcriptome research on H. pylori biofilms remains limited [6–9]
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