Neutrophil antimicrobial proteins enhance Shigella flexneri adhesion and invasion |
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| Authors: | Björn Eilers Anne Mayer‐Scholl Travis Walker Christoph Tang Yvette Weinrauch Arturo Zychlinsky |
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| Institution: | 1. Department of Cellular Microbiology, Max‐Planck‐Institute for Infection Biology, Chariteplatz 1, 10117 Berlin, Germany.;2. Present address: Bundesinstitut für Risikobewertung (BfR), Diedersdorfer Weg 1, 12277 Berlin, Germany;3. Department of Microbiology, School of Medicine, New York University, 10016 New York, USA.;4. Department of General Surgery, University of Colorado Denver, Aurora, CO 80045, USA.;5. Department of Infectious Diseases, Faculty of Medicine, Centre for Molecular Microbiology and Infection, Flowers Building, Imperial College London, London SW7 2AZ, UK. |
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| Abstract: | 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. |
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