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Infect Immun, May 1998, p. 1878-1884, Vol. 66, No. 5
Microbial Pathogenesis Unit, Christian de
Duve Institute of Cellular Pathology, and Faculté de
Médecine, Université Catholique de Louvain, B-1200
Brussels, Belgium
Received 6 November 1997/Returned for modification 23 December
1997/Accepted 12 February 1998
The Yersinia plasmid-encoded Yop virulon enables
extracellular adhering bacteria to deliver toxic effector proteins
inside their target cells. It includes a type III secretion system
(Ysc), at least two translocator proteins (YopB, YopD), and a set of intracellular Yop effectors (YopE, YopH, YopO, YopM, and YopP). Infection of macrophages with a wild-type strain leads to low levels of tumor necrosis factor alpha (TNF-
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Copyright © 1998, American Society for Microbiology. All rights reserved.
Role of YopP in Suppression of Tumor Necrosis
Factor Alpha Release by Macrophages during Yersinia
Infection
) release compared to
infection with plasmid-cured strains, suggesting that the virulence plasmid encodes a factor impairing the normal TNF-
response of infected macrophages. This effect is correlated with the inhibition of
the macrophage mitogen-activated protein kinase (MAPK) activities. To
identify the Yop protein responsible for the suppression of TNF-
release, we infected J774A.1 and PU5-1.8 macrophages with a battery of
knockout Yersinia enterocolitica mutants and we quantified the TNF-
released. Mutants affected in secretion (yscN),
in translocation (yopB and yopD), or in
synthesis of all the known Yop effectors (yopH,
yopO, yopP, yopE, and
yopM polymutants) were unable to block the TNF-
response
of the macrophages. In contrast, single yopE,
yopH, yopO, and yopM mutants
behaved like the wild-type strain. A yopP mutant elicited
elevated TNF-
release, and complementation of the yopP
mutant or the yop effector polymutant strain with yopP alone led to a drop in TNF-
release. In addition,
YopP was also responsible for the inhibition of the extracellular
signal-regulated kinase2 (ERK2) and p38 MAPK activities. These
results show that YopP is the Yop effector responsible for the
Yersinia-induced suppression of TNF-
release by infected
macrophages.
*
Corresponding author. Mailing address: Microbial
Pathogenesis Unit, Avenue Hippocrate, 74, UCL Box 74-49, B-1200
Brussels, Belgium. Phone: 32 2 764 74 49. Fax: 32 2 764 74 98. E-mail:
Cornelis{at}mipa.ucl.ac.be.
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