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Infection and Immunity, May 1999, p. 2567-2574, Vol. 67, No. 5
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Yersinia pseudotuberculosis-Induced Calcium Signaling in Neutrophils Is Blocked by the Virulence Effector YopH

Kerstin Andersson,1,* Karl-Eric Magnusson,1 Meytham Majeed,1,dagger Olle Stendahl,1 and Maria Fällman2

Division of Medical Microbiology, Department of Health and Environment, Linköping University, SE-581 85 Linköping,1 and Department of Cell and Molecular Biology, University of Umeå, SE-901 87 Umeå,2 Sweden

Received 29 October 1998/Returned for modification 7 December 1998/Accepted 12 February 1999

Pathogenic species of the genus Yersinia evade the bactericidal functions of phagocytes. This evasion is mediated through their virulence effectors, Yops, which act within target cells. In this study we investigated the effect of Yersinia pseudotuberculosis on Ca2+ signaling in polymorphonuclear neutrophils. The intracellular free calcium concentration in single adherent human neutrophils was monitored during bacterial infection and, in parallel, the encounter between the bacteria and cells was observed. When a plasmid-cured strain was used for infection, adherence of a single bacterium to the cellular surface induced a beta 1 integrin-dependent transient increase in the intracellular concentration of free calcium. This was, however, not seen with Yop-expressing wild-type bacteria, which adhered to the cell surface without generating any Ca2+ signal. Importantly, the overall Ca2+ homeostasis was not affected by the wild-type strain; the Ca2+ signal mediated by the G-protein-coupled formyl-methionyl-leucyl-phenylalanine receptor was still functioning. Hence, the blocking effect was restricted to certain receptors and their signaling pathways. The use of different Yop mutant strains revealed that the protein tyrosine phosphatase YopH was responsible for the inhibition. This virulence determinant has previously been implicated in very rapid Yersinia-mediated effects on target cells as the key effector in the blockage of phagocytic uptake. The present finding, that Y. pseudotuberculosis, via YopH, specifically inhibits a self-induced immediate-early Ca2+ signal in neutrophils, offers more-detailed information concerning the effectiveness of this virulence effector and implies an effect on Ca2+-dependent, downstream signals.

* Corresponding author. Mailing address: Division of Medical Microbiology, Department of Health and Environment, Linköping University, SE-581 85 Linköping, Sweden. Phone: 46-13-222059. Fax: 46-13-224789. E-mail: keran{at}mme.liu.se.

dagger Present address: Institute of General Pathology, University of Verona, 37134 Verona, Italy.

Infection and Immunity, May 1999, p. 2567-2574, Vol. 67, No. 5
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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