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Infection and Immunity, September 2006, p. 5126-5131, Vol. 74, No. 9
0019-9567/06/$08.00+0     doi:10.1128/IAI.00219-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Yersinia pestis YopJ Suppresses Tumor Necrosis Factor Alpha Induction and Contributes to Apoptosis of Immune Cells in the Lymph Node but Is Not Required for Virulence in a Rat Model of Bubonic Plague

Nadine Lemaître,1,2,{dagger} Florent Sebbane,1,{dagger},{ddagger} Daniel Long,3 and B. Joseph Hinnebusch1*

Laboratory of Zoonotic Pathogens,1 Veterinary Branch,3 Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, Inserm U801, Lille F-50921, Université de Lille II, Faculté de Médecine Henri Warembourg, Lille F-59045, Institut Pasteur de Lille, Lille F-59021, France2

Received 8 February 2006/ Returned for modification 23 March 2006/ Accepted 2 June 2006

The virulence of the pathogenic Yersinia species depends on a plasmid-encoded type III secretion system that transfers six Yop effector proteins into host cells. One of these proteins, YopJ, has been shown to disrupt host cell signaling pathways involved in proinflammatory cytokine production and to induce macrophage apoptosis in vitro. YopJ-dependent apoptosis in mesenteric lymph nodes has also been demonstrated in a mouse model of Yersinia pseudotuberculosis infection. These results suggest that YopJ attenuates the host innate and adaptive immune response during infection, but the role of YopJ during bubonic plague has not been completely established. We evaluated the role of Yersinia pestis YopJ in a rat model of bubonic plague following intradermal infection with a fully virulent Y. pestis strain and an isogenic yopJ mutant. Deletion of yopJ resulted in a twofold decrease in the number of apoptotic immune cells in the bubo and a threefold increase in serum tumor necrosis factor alpha levels but did not result in decreased virulence, systemic spread, or colonization levels in the spleen and blood. Our results indicate that YopJ is not essential for bubonic plague pathogenesis, even after peripheral inoculation of low doses of Y. pestis. Instead, the effects of YopJ appear to overlap and augment the immunomodulatory effects of other Y. pestis virulence factors.

* Corresponding author. Mailing address: Rocky Mountain Laboratories, NIAID, NIH, 903 S. 4th St., Hamilton, MT 59840. Phone: (406) 363-9260. Fax: (406) 363-9394. E-mail: jhinnebusch{at}niaid.nih.gov.

Editor: J. B. Bliska

{dagger} N.L. and F.S. contributed equally to this work.

{ddagger} Present addresses: Inserm U801, Lille F-59021, France; Université de Lille II, Lille F-59800, France; and Institut Pasteur de Lille, Lille, F-59021, France.

Infection and Immunity, September 2006, p. 5126-5131, Vol. 74, No. 9
0019-9567/06/$08.00+0     doi:10.1128/IAI.00219-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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