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Salmonella pathogenicity island 2-dependent evasion of the phagocyte NADPH oxidase
被引:432
|作者:
Vazquez-Torres, A
Xu, YS
Jones-Carson, J
Holden, DW
Lucia, SM
Dinauer, MC
Mastroeni, P
Fang, FC
[1
]
机构:
[1] Univ Colorado, Hlth Sci Ctr, Dept Med, Denver, CO 80262 USA
[2] Univ Colorado, Hlth Sci Ctr, Dept Pathol, Denver, CO 80262 USA
[3] Univ Colorado, Hlth Sci Ctr, Dept Microbiol, Denver, CO 80262 USA
[4] Univ London Imperial Coll Sci Technol & Med, Sch Med, Dept Infect Dis, London W12 0NN, England
[5] Indiana Univ, Sch Med, Indianapolis, IN 46202 USA
[6] Univ London Imperial Coll Sci Technol & Med, Dept Biochem, London SW7 2BZ, England
来源:
关键词:
D O I:
10.1126/science.287.5458.1655
中图分类号:
O [数理科学和化学];
P [天文学、地球科学];
Q [生物科学];
N [自然科学总论];
学科分类号:
07 ;
0710 ;
09 ;
摘要:
A type III protein secretion system encoded by Salmonella pathogenicity island 2 (SPI2) has been found to be required for virulence and survival within macrophages. Here, SPI2 was shown to allow Salmonella typhimurium to avoid NADPH oxidase-dependent killing by macrophages. The ability of SPI2-mutant bacteria to survive in macrophages and to cause Lethal infection in mice was restored by abrogation of the NADPH oxidase-dependent respiratory burst. Ultrastructural and immunofluorescence microscopy demonstrated efficient Localization of the NADPH oxidase in the proximity of vacuoles containing SPI2-mutant but not wild-type bacteria, suggesting that SPI2 interferes with trafficking of oxidase-containing vesicles to the phagosome.
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页码:1655 / 1658
页数:4
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