Abstract
Background. The carbohydrates of gastric mucins and other sugar structures are involved in interactions with Helicobacter pylori (H. pylori) adhesins. The binding of bacteria to mucins can protect the epithelium from direct contact with the pathogen and from developing infection because of a specific barrier created by the mucus. The pathogen also interacts with other carbohydrate structures of the epithelium. Direct contact between the bacteria and the epithelial cells facilitates infection development. Objectives. The aim of this study was to assess the influence of Maackia amurensis (MAA), Lotus tetragonolobus (LTA), Ulex europaeus (UEA), and Arachis hypogaea (PNA) lectins on the binding of gastric carbohydrates with H. pylori adhesins. Material and methods. Three patients’ gastric juices and 12 H. pylori strains were included in the study. An ELISA test was used to assess the presence of MUC1 and MUC5AC mucins and the sugar structures recognized by all examined lectins. The binding of the bacterium to the sugar structures was analyzed by the ELISA method with and without the gastric juices pretreated with lectins. Results. In the majority of the samples examined, MAA, LTA, UEA, and PNA lectins enhanced the binding of H. pylori to specific carbohydrate structures of gastric mucins. Conclusions. Substances which influence the binding of the pathogen with specific carbohydrate receptors on gastric epithelial cells can favor inflammation development. However, if H. pylori binds with mucins, the bacterium can have difficulty reaching the epithelium and progressing with infection.
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Radziejewska, I., Borzym-Kluczyk, M., & Leszczynska, K. (2018). Lotus tetragonolobus, Ulex europaeus, Maackia amurensis, and Arachis hypogaea (peanut) lectins influence the binding of Helicobacter pylori to gastric carbohydrates. Advances in Clinical and Experimental Medicine, 27(6), 807–811. https://doi.org/10.17219/acem/68987
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