Abstract
Resistance to bile acids is a necessary ability for bacteria that live in the gastrointestinal tract, such as Helicobacter pylori. The role of the bacterial drug efflux system is important for bile acid tolerance. Using the H. pylori JP26 strain and the JP26AcrB strain deficient in AcrB the relationship between the drug efflux system AcrB and the bile acid tolerance of H. pylori was investigated. Bacterial susceptibility to bile acids was measured by the agar dilution method. To examine the ability to efflux bile acids, the intracellular accumulation of radiolabeled chenodeoxycholic acid was measured with a liquid scintillation counter. To investigate the effect of bile acid on the cell adhesion ability of bacteria, bacteria were attached to AGS cells supplemented with chenodeoxycholic acid, and the number of bacteria was counted. Bile acid resistance was significantly lower in the AcrB mutant than in the wild-type strain. The AcrB mutant strains showed a significant increase in the accumulation of 14C - labeled chenodeoxycholic acid in the bacteria. In terms of attachment to AGS cells, the AcrB mutant was significantly lower than the wild-type strain. Furthermore, the AcrB mutant with chenodeoxycholic acid could not be identified. Our results reveal that H. pylori AcrB plays an important role in bile acid resistance. We also suggest that drugs targeting the AcrB efflux system may be a new treatment for H. pylori.
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