The V-antigen of Yersinia is surface exposed before target cell contact and involved in virulence protein translocation

被引:181
作者
Pettersson, J
Holmström, A
Hill, J
Leary, S
Frithz-Lindsten, E
von Euler-Matell, A
Carlsson, E
Titball, R
Forsberg, Å
Wolf-Watz, H [1 ]
机构
[1] Umea Univ, Dept Cell & Mol Biol, S-90187 Umea, Sweden
[2] Def Res Estab, Dept Microbiol, S-90182 Umea, Sweden
[3] Def Evaluat & Res Agcy, Dept Biomed Sci, Salisbury SP4 0JQ, Wilts, England
[4] Karolinska Inst, Ctr Microbiol & Tumor Biol, S-17177 Stockholm, Sweden
[5] Umea Univ, Dept Anat, S-90187 Umea, Sweden
关键词
D O I
10.1046/j.1365-2958.1999.01408.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Type Ill-mediated translocation of Yop effecters is an essential virulence mechanism of pathogenic Yersinia. LcrV is the only protein secreted by the type III secretion system that induces protective immunity. LcrV also plays a significant role in the regulation of Yop expression and secretion. The role of LcrV in the virulence process has, however, remained elusive on account of its pleiotropic effects. Here, we show that anti-LcrV antibodies can block the delivery of Yop effecters into the target cell cytosol. This argues strongly for a critical role of LcrV in the Yop translocation process. Additional evidence supporting this role was obtained by genetic analysis. LcrV was found to be present on the bacterial surface before the establishment of bacteria target cell contact. These findings suggest that LcrV serves an important role in the initiation of the translocation process and provides one possible explanation for the mechanism of kcrV-induced protective immunity.
引用
收藏
页码:961 / 976
页数:16
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