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Infection and Immunity, September 2009, p. 3791-3806, Vol. 77, No. 9
0019-9567/09/$08.00+0     doi:10.1128/IAI.00284-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Gr1+ Cells Control Growth of YopM-Negative Yersinia pestis during Systemic Plague{triangledown}

Zhan Ye,1 Edward J. Kerschen,1,{dagger} Donald A. Cohen,1 Alan M. Kaplan,1 Nico van Rooijen,2 and Susan C. Straley1*

Department of Microbiology, Immunology, and Molecular Genetics, University of Kentucky, Lexington, Kentucky 40536-0298,1 Department of Molecular Cell Biology, Vrije Universiteit Medical Center, Faculty of Medicine, Van der Boechorststraat 7, 1081 BT Amsterdam, The Netherlands2

Received 11 March 2009/ Returned for modification 24 March 2009/ Accepted 24 June 2009

YopM, a protein toxin of Yersinia pestis, is necessary for virulence in a mouse model of systemic plague. We previously reported YopM-dependent natural killer (NK) cell depletion from blood and spleen samples of infected mice. However, in this study we found that infection with Y. pestis KIM5 (YopM+) caused depletion of NK cells in the spleen, but not in the liver, and antibody-mediated ablation of NK cells had no effect on bacterial growth. There was no YopM-associated effect on the percentage of dendritic cells (DCs) or polymorphonuclear leukocytes (PMNs) in the early stage of infection; however, there was a YopM-associated effect on PMN integrity and on the influx of monocytes into the spleen. Ablation of Gr1+ cells caused loss of the growth defect of YopM– Y. pestis in both the liver and spleen. In contrast, ablation of macrophages/DCs inhibited growth of both parent and mutant bacteria, accompanied by significantly fewer lesion sites in the liver. These results point toward PMNs and inflammatory monocytes as major cell types that control growth of YopM– Y. pestis. Infection with fully virulent Y. pestis CO92 and a YopM– derivative by intradermal and intranasal routes showed that the absence of YopM significantly increased the 50% lethal dose only in the intradermal model, suggesting a role for YopM in bubonic plague, in which acute inflammation occurs soon after infection.

* Corresponding author. Mailing address: Department of Microbiology, Immunology, and Molecular Genetics, University of Kentucky, Lexington, KY 40536-0298. Phone: (859) 323-6538. Fax: (859) 257-8994. E-mail: scstra01{at}uky.edu

{triangledown} Published ahead of print on 6 July 2009.

Editor: J. B. Bliska

{dagger} Present address: Blood Center of Southeastern Wisconsin, Inc., 638 N. 18th Street, Milwaukee, WI 53201-2178.

Infection and Immunity, September 2009, p. 3791-3806, Vol. 77, No. 9
0019-9567/09/$08.00+0     doi:10.1128/IAI.00284-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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