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Shigella flexneri is an enteric pathogen that causes massive inflammation and destruction of the human intestinal epithelium. Neutrophils are the first cells of the innate immune system recruited to the site of infection. These cells can attack microbes by phagocytosis, Neutrophil Extracellular Trap (NET) formation and degranulation. Here, we investigated how neutrophil degranulation affects virulence and show that exposure of Shigella to granular proteins enhances infection of epithelial cells. During this process, cationic granular proteins bind to the Shigella surface causing increased adhesion which ultimately leads to hyperinvasion. This effect is mediated by changes in the surface charge, since a lipopolysaccharide (LPS) mutant with a negative surface shows enhanced hyperinvasion compared with wild-type Shigella. We propose that Shigella evolved to use host defence molecules to enhance its virulence and subvert the innate immune system.

Original publication

DOI

10.1111/j.1462-5822.2010.01459.x

Type

Journal article

Journal

Cell Microbiol

Publication Date

08/2010

Volume

12

Pages

1134 - 1143

Keywords

Antimicrobial Cationic Peptides, Bacterial Adhesion, Colony Count, Microbial, Epithelial Cells, HeLa Cells, Humans, Immune Evasion, Microbial Viability, Neutrophils, Shigella flexneri