Shigella flexneri phagosomal escape is independent of invasion.
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.
Department of Cellular Microbiology, Max-Planck-Institut für Infektionsbiologie, Charité Platz 1, D-10117 Berlin, Germany.
Susanne
S
Paetzold
Sebastian
S
Lourido
Bärbel
B
Raupach
Arturo
A
Zychlinsky
D000818:Animals; D004847:Epithelial Cells / Q000382:microbiology; D017353:Gene Deletion; D005816:Genetic Complementation Test; D044404:Genomic Islands / Q000235:genetics; D006367:HeLa Cells; D006801:Humans; D051379:Mice; D010586:Phagocytes / Q000382:microbiology; D010588:Phagosomes / Q000382:microbiology*; D010957:Plasmids / Q000235:genetics; D012486:Salmonella typhimurium / Q000235:genetics; D012763:Shigella flexneri / Q000235:genetics / Q000276:immunology* / Q000472:pathogenicity*; D014774:Virulence / Q000235:genetics*; D037521:Virulence Factors / Q000235:genetics*
D037521:Virulence Factors