PI5P Triggers ICAM-1 Degradation in Shigella Infected Cells, Thus Dampening Immune Cell Recruitment

Cell Reports
Frédéric BoalHélène Tronchère

Abstract

Shigella flexneri, the pathogen responsible for bacillary dysentery, has evolved multiple strategies to control the inflammatory response. Here, we show that Shigella subverts the subcellular trafficking of the intercellular adhesion molecule-1 (ICAM-1), a key molecule in immune cell recruitment, in a mechanism dependent on the injected bacterial enzyme IpgD and its product, the lipid mediator PI5P. Overexpression of IpgD, but not a phosphatase dead mutant, induced the internalization and the degradation of ICAM-1 in intestinal epithelial cells. Remarkably, addition of permeant PI5P reproduced IpgD effects and led to the inhibition of neutrophil recruitment. Finally, these results were confirmed in an in vivo model of Shigella infection where IpgD-dependent ICAM-1 internalization reduced neutrophil adhesion. In conclusion, we describe here an immune evasion mechanism used by the pathogen Shigella to divert the host cell trafficking machinery in order to reduce immune cell recruitment.

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Citations

Apr 12, 2018·Journal of Innate Immunity·Scott D KobayashiFrank R DeLeo
Jul 14, 2017·The EMBO Journal·Chun Hui SunGuy Tran Van Nhieu
Mar 18, 2017·Cell Structure and Function·Junya HasegawaLois S Weisman
May 1, 2019·International Journal of Molecular Sciences·Alessandro PoliNullin Divecha
Mar 16, 2021·Frontiers in Cell and Developmental Biology·Tiffany G RoachDaniel G S Capelluto
Apr 7, 2019·Microbiology Spectrum·Pamela Schnupf, Philippe J Sansonetti

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