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

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...

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Main Authors:	Frédéric Boal, Andrea Puhar, Jean-Marie Xuereb, Oksana Kunduzova, Philippe J. Sansonetti, Bernard Payrastre, Hélène Tronchère
Format:	Article
Language:	English
Published:	Elsevier 2016-02-01
Series:	Cell Reports
Online Access:	http://www.sciencedirect.com/science/article/pii/S2211124715015351

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spelling	doaj-3aca905d486d4e6cae0af692a17bb6e12020-11-25T00:43:11ZengElsevierCell Reports2211-12472016-02-0114475075910.1016/j.celrep.2015.12.079PI5P Triggers ICAM-1 Degradation in Shigella Infected Cells, Thus Dampening Immune Cell RecruitmentFrédéric Boal0Andrea Puhar1Jean-Marie Xuereb2Oksana Kunduzova3Philippe J. Sansonetti4Bernard Payrastre5Hélène Tronchère6INSERM U1048, I2MC and Université Paul Sabatier, 31432 Toulouse, FranceINSERM U1202, Unité de Pathogénie Microbienne Moléculaire, Institut Pasteur, 75724 Paris Cedex 15, FranceINSERM U1048, I2MC and Université Paul Sabatier, 31432 Toulouse, FranceINSERM U1048, I2MC and Université Paul Sabatier, 31432 Toulouse, FranceINSERM U1202, Unité de Pathogénie Microbienne Moléculaire, Institut Pasteur, 75724 Paris Cedex 15, FranceINSERM U1048, I2MC and Université Paul Sabatier, 31432 Toulouse, FranceINSERM U1048, I2MC and Université Paul Sabatier, 31432 Toulouse, FranceShigella 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.http://www.sciencedirect.com/science/article/pii/S2211124715015351
collection	DOAJ
language	English
format	Article
sources	DOAJ
author	Frédéric Boal Andrea Puhar Jean-Marie Xuereb Oksana Kunduzova Philippe J. Sansonetti Bernard Payrastre Hélène Tronchère
spellingShingle	Frédéric Boal Andrea Puhar Jean-Marie Xuereb Oksana Kunduzova Philippe J. Sansonetti Bernard Payrastre Hélène Tronchère PI5P Triggers ICAM-1 Degradation in Shigella Infected Cells, Thus Dampening Immune Cell Recruitment Cell Reports
author_facet	Frédéric Boal Andrea Puhar Jean-Marie Xuereb Oksana Kunduzova Philippe J. Sansonetti Bernard Payrastre Hélène Tronchère
author_sort	Frédéric Boal
title	PI5P Triggers ICAM-1 Degradation in Shigella Infected Cells, Thus Dampening Immune Cell Recruitment
title_short	PI5P Triggers ICAM-1 Degradation in Shigella Infected Cells, Thus Dampening Immune Cell Recruitment
title_full	PI5P Triggers ICAM-1 Degradation in Shigella Infected Cells, Thus Dampening Immune Cell Recruitment
title_fullStr	PI5P Triggers ICAM-1 Degradation in Shigella Infected Cells, Thus Dampening Immune Cell Recruitment
title_full_unstemmed	PI5P Triggers ICAM-1 Degradation in Shigella Infected Cells, Thus Dampening Immune Cell Recruitment
title_sort	pi5p triggers icam-1 degradation in shigella infected cells, thus dampening immune cell recruitment
publisher	Elsevier
series	Cell Reports
issn	2211-1247
publishDate	2016-02-01
description	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.
url	http://www.sciencedirect.com/science/article/pii/S2211124715015351
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PI5P Triggers ICAM-1 Degradation in Shigella Infected Cells, Thus Dampening Immune Cell Recruitment

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