SseA is required for translocation of Salmonella pathogenicity island-2 effectors into host cells

• Published in: Microbes and infection Vol. 5; no. 7; pp. 561 - 570
• Main Authors: Coombes, Brian K., Brown, Nat F., Kujat-Choy, Sonya, Vallance, Bruce A., Finlay, B.Brett
• Format: Journal Article
• Language: English
• Published: Lausanne Elsevier SAS 01.06.2003; Amsterdam Elsevier; Paris
• Subjects: Animals; Bacterial Proteins - genetics; Bacterial Proteins - metabolism; Bacteriology; Biological and medical sciences; Female; Fundamental and applied biological sciences. Psychology; Genes, Bacterial; HeLa Cells; Humans; Membrane Proteins - genetics; Membrane Proteins - metabolism; Mice; Mice, Inbred BALB C; Microbiology; Molecular Chaperones - genetics; Molecular Chaperones - physiology; Mutation; Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains; Protein Transport; Salmonella - metabolism; Salmonella - pathogenicity; Salmonella enterica serovar Typhimurium; Salmonella Infections, Animal - microbiology; Salmonella pathogenicity island-2; Type III secretion; Virulence factor; Virulence Factors - physiology; Salmonella pathogenicity island-2; Salmonella enterica serovar Typhimurium; Type III secretion; Virulence factor; Secretion; Virulence; Pathogenicity island; Salmonella typhimurium; Mechanism; Pathogenicity; Bacteria; Attenuated strain; Enterobacteriaceae
• ISSN: 1286-4579; 1769-714X
• DOI: 10.1016/S1286-4579(03)00094-7

The Salmonella pathogenicity island-2 (SPI2) is a virulence locus on the bacterial chromosome required for intracellular proliferation and systemic infection in mice. Cell culture models and a murine model of systemic infection were used to address the role of an uncharacterized SPI2 open reading frame, designated as sseA, in Salmonella virulence. A Salmonella strain with an unmarked internal deletion of sseA displayed a phenotype that was similar to an SPI2-encoded type III secretion system apparatus mutant. Moreover, SseA was required for survival and replication within epithelial cells and macrophages. Murine infection studies confirmed that the ΔsseA strain was severely attenuated for virulence. Using immunofluorescence microscopy, the virulence defect in the ΔsseA strain was attributed to an inability to translocate SPI2 effector proteins into host cells. These data demonstrate that SseA is essential for SPI2-mediated translocation of effector proteins.