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Gastric Colonization by H. pylori

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Abstract

Helicobacter pylori (H. pylori) is uniquely adapted to colonize the gastric mucosa. The key components for gastric colonization include motility, adhesion, and acid acclimation. The flagellar system allows the bacteria to move within the gastric mucus layer to the sites where conditions are optimal for survival. Adhesion to the gastric mucosa, via interaction between bacterial and host proteins, allows the bacteria to withstand bulk flow of gastric fluid. Acid acclimation is the system that allows for periplasmic and cytoplasmic pH regulation in the setting of an acidic environment. The bacteria are bioenergetically neutralophiles, meaning they are able to survive between pH 4 and 8 and grow between pH 6 and 8. The pH at the gastric surface in the presence of H. pylori, as shown by microelectrode, fluorescent dye, and in vivo transcriptome studies, is below the range for growth and near to below the limits for survival. The bacteria are able to sense acidic medium pH and stimulate trafficking of cytoplasmic urease and its accessory proteins to the proton-gated urea channel, UreI, in the inner membrane. The breakdown of urea into carbon dioxide and ammonia buffers the periplasm and cytoplasm to within the pH range optimal for a neutralophile. Understanding gastric colonization is clinically relevant because these systems that facilitate colonization can be targeted or interfered with to improve efficacy of eradication regimens.

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Marcus, E.A., Scott, D.R. (2016). Gastric Colonization by H. pylori . In: Kim, N. (eds) Helicobacter pylori. Springer, Singapore. https://doi.org/10.1007/978-981-287-706-2_2

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