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Shigella, the leading cause of bacillary dysentery, uses a type III secretion system (TTSS) to inject proteins into human cells, leading to bacterial invasion and a vigorous inflammatory response. The bacterium is protected against the response by the O antigen of lipopolysaccharide (LPS) on its surface. We show that bacteriophage-encoded glucosylation of Shigella O antigen, the basis of different serotypes, shortens the LPS molecule by around half. This enhances TTSS function without compromising the protective properties of the LPS. Thus, LPS glucosylation promotes bacterial invasion and evasion of innate immunity, which may have contributed to the emergence of serotype diversity in Shigella.

Original publication




Journal article



Publication Date





1313 - 1317


Animals, Bacterial Adhesion, Bacteriophages, Carbohydrate Conformation, Dysentery, Bacillary, Glucose, Glycosylation, Hydrophobic and Hydrophilic Interactions, Immunity, Innate, Intestinal Mucosa, Lipopolysaccharides, Microscopy, Electron, Scanning, Microscopy, Electron, Transmission, Mutation, Neutrophils, O Antigens, Operon, Rabbits, Serotyping, Shigella flexneri, Virulence