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Reduced apoptosis of mouse macrophages induced by yscW mutant of Yersinia pestis results from the reduced secretion of YopJ and relates to caspase-3 signal pathway.

Abstract：

:The virulence of the pathogenic Yersinia species depends on a plasmid-encoded type III secretion system (T3SS) that injects six Yersinia outer protein (Yop) effector proteins into the cytosol of macrophages, leading to disruption of host defence mechanisms. Here, we report that a T3SS structural protein YscW of Yersinia pestis contributed to the induction of apoptosis of murine macrophages. The apoptotic percentage of macrophages, from both mouse peritoneal cavity and spleen, and of RAW264.7 cell line, caused by the yscW mutant strain was significantly lower than that by wild type (WT) Y. pestis and yscW complemented strain. Meanwhile, detection of caspase-3 activity in macrophages, a key apoptosis-inducing protein, showed coincident results with the changes of macrophage apoptosis induced by WT, yscW mutant and complemented strains, indicating that macrophage apoptosis was related to caspase-3 signal pathways. However, ectopic expression of YscW in RAW264.7 cells cannot increase the macrophage apoptosis and death, suggesting that YscW itself could not induce macrophage apoptosis directly. To get insight into the mechanism of this phenomenon, we investigated the secretion of YopJ, which has been thought to be the only Yop effector related to apoptosis, in WT, mutant and complemented strains, respectively. Results showed that in yscW mutant strain, secretion of YopJ was decreased significantly in the supernatant than that in WT or complemented strain. This means although YscW does not induce apoptosis directly, it can indirectly affect apoptosis through reducing the secretion of YopJ.

journal_name

Scand J Immunol

journal_title

Scandinavian journal of immunology

authors

Bi Y,Du Z,Yang H,Guo Z,Tan Y,Zhu Z,Yang R

doi

10.1111/j.1365-3083.2009.02297.x

subject

Has Abstract

pub_date

2009-10-01 00:00:00

pages

358-67

issue

4

eissn

0300-9475

issn

1365-3083

pii

SJI2297

journal_volume

70

pub_type

杂志文章

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