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Infection and Immunity, October 2007, p. 4826-4830, Vol. 75, No. 10
0019-9567/07/$08.00+0 doi:10.1128/IAI.00454-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Sebastian Lourido,
,
Bärbel Raupach, and
Arturo Zychlinsky*
Department of Cellular Microbiology, Max-Planck-Institut für Infektionsbiologie, Charité Platz 1, D-10117 Berlin, Germany
Received 28 March 2007/ Returned for modification 17 May 2007/ Accepted 17 July 2007
Infections with Salmonella enterica serovar Typhimurium and Shigella flexneri result in mucosal inflammation in response to epithelial cell invasion and macrophage cytotoxicity. These processes are mediated by type III secretion systems encoded in homologous virulence loci in the two species, namely, Salmonella pathogenicity island 1 (SPI-1), carried in the genome, and the Shigella entry region (SER), carried in a large virulence plasmid. Here we show that SPI-1 can functionally complement a deletion of SER in S. flexneri, restoring invasion of epithelial cells, macrophage cytotoxicity, and phagosomal escape. Furthermore, S. flexneri phagosomal escape requires the SER and another gene(s) carried on the large virulence plasmid. We demonstrate that the processes of invasion and phagosomal escape can be uncoupled in S. flexneri.
Published ahead of print on 30 July 2007.
S.P. and S.L. contributed equally to this study.
Present address: Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, MO 63130.
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