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Max von Pettenkofer-Institut für Hygiene und Medizinische Mikrobiologie, Munich, Germany
The virulence-associated V Ag (LcrV) of pathogenic
Yersinia species is part of the translocation apparatus,
required to deliver antihost effector proteins (Yersinia
outer proteins) into host cells. An orthologous protein (denoted as
PcrV) has also been identified in the ExoS regulon of
Pseudomonas aeruginosa. Additionally, it is known that
LcrV is released by yersiniae into the environment and that LcrV causes
an immunosuppressive effect when injected into mice. In this study, we
demonstrate for the first time that rLcrV, but not PcrV, is capable of
suppressing TNF-
production in zymosan A-stimulated mouse
macrophages and the human monocytic Mono-Mac-6 cell line. The
underlying mechanism of TNF- suppression could be assigned to
LcrV-mediated IL (IL)-10 production, because 1) LcrV induces IL-10
release in macrophages, 2) anti-IL-10 Ab treatment completely
abrogated TNF- suppression, and 3) TNF- suppression was absent in
LcrV-treated macrophages of IL-10-deficient (IL-10-/-)
mice. The relevance of LcrV-mediated immunosuppression for the
pathogenicity of yersiniae became evident by experimental infection of
mice; in contrast to wild-type mice, IL-10-/- mice were
highly resistant against Yersinia infection, as shown by
lower bacterial load in spleen and liver, absent abscess formation in
these organs, and survival.
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