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PI5P Triggers ICAM-1 Degradation in Shigella Infected Cells, Thus Dampening Immune Cell Recruitment
INSERM U1048, I2MC and Universite´ Paul Sabatier, 31432 Toulouse, France.
Umeå universitet, Medicinska fakulteten, Molekylär Infektionsmedicin, Sverige (MIMS). Umeå universitet, Medicinska fakulteten, Umeå Centre for Microbial Research (UCMR). Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten). INSERM U1202, Unite´ de Pathogénie Microbienne Moléculaire, Institut Pasteur, 75724 Paris Cedex 15, France. (Andrea Puhar)ORCID-id: 0000-0002-9915-002X
INSERM U1048, I2MC and Universite´ Paul Sabatier, 31432 Toulouse, France.
INSERM U1048, I2MC and Universite´ Paul Sabatier, 31432 Toulouse, France.
Vise andre og tillknytning
2016 (engelsk)Inngår i: Cell Reports, E-ISSN 2211-1247, Vol. 14, nr 4, s. 750-759Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

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.

sted, utgiver, år, opplag, sider
Cell Press , 2016. Vol. 14, nr 4, s. 750-759
HSV kategori
Forskningsprogram
infektionssjukdomar
Identifikatorer
URN: urn:nbn:se:umu:diva-115891DOI: 10.1016/j.celrep.2015.12.079ISI: 000369104500007PubMedID: 26776508Scopus ID: 2-s2.0-84958125208OAI: oai:DiVA.org:umu-115891DiVA, id: diva2:900958
Tilgjengelig fra: 2016-02-05 Laget: 2016-02-05 Sist oppdatert: 2024-01-17bibliografisk kontrollert

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