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DOI 10.1038/s41598-024-59234-w

Медицинская библиотека · Scientific reports · 2024

Probing the expression and adhesion of glycans involved in Helicobacter pylori infection.

Sijmons Daniel, Collett Simon, Soliman Caroline, Guy Andrew J, Scott Andrew M, Durrant Lindy G, Elbourne Aaron, Walduck Anna K, Ramsland Paul A

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Аннотация

Helicobacter pylori infects approximately half the human population and has an unusual infective niche of the human stomach. Helicobacter pylori is a major cause of gastritis and has been classified as a group 1 carcinogen by the WHO. Treatment involves triple or quadruple antibiotic therapy, but antibiotic resistance is becoming increasingly prevalent. Helicobacter pylori expresses certain blood group related antigens (Lewis system) as a part of its lipopolysaccharide (LPS), which is thought to assist in immune evasion. Additionally, H. pylori LPS participates in adhesion to host cells alongside several adhesion proteins. This study profiled the carbohydrates of H. pylori reference strains (SS1 and 26695) using monoclonal antibodies (mAbs) and lectins, identifying interactions between two carbohydrate-targeting mAbs and multiple lectins. Atomic force microscopy (AFM) scans were used to probe lectin and antibody interactions with the bacterial surfaces. The selected mAb and lectins displayed an increased adhesive force over the surface of the curved H. pylori rods. Furthermore, this study demonstrates the ability of anti-carbohydrate antibodies to reduce the adhesion of H. pylori 26695 to human gastric adenocarcinoma cells via AFM. Targeting bacterial carbohydrates to disrupt crucial adhesion and immune evasion mechanisms represents a promising strategy for combating H. pylori infection.

Для цитирования: Sijmons Daniel, Collett Simon, Soliman Caroline, Guy Andrew J, Scott Andrew M, Durrant Lindy G, Elbourne Aaron, Walduck Anna K, Ramsland Paul A. Probing the expression and adhesion of glycans involved in Helicobacter pylori infection.. Scientific reports. 2024. DOI: 10.1038/s41598-024-59234-w.

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