This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bubeck, S. S.
Right arrow Articles by Dube, P. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bubeck, S. S.
Right arrow Articles by Dube, P. H.

 Previous Article  |  Next Article 

Infection and Immunity, February 2007, p. 697-705, Vol. 75, No. 2
0019-9567/07/$08.00+0     doi:10.1128/IAI.00403-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Delayed Inflammatory Response to Primary Pneumonic Plague Occurs in Both Outbred and Inbred Mice{triangledown}

Sarah S. Bubeck, Angelene M. Cantwell, and Peter H. Dube*

Department of Microbiology and Immunology, The University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr., San Antonio, Texas 78229

Received 13 March 2006/ Returned for modification 12 April 2006/ Accepted 3 November 2006

Yersinia pestis is the causative agent of plague, a disease that can manifest as either bubonic or pneumonic plague. An interesting feature of plague is that it is a rapidly progressive disease, suggesting that Y. pestis either evades and/or suppresses the innate immune response to infection. Therefore, the early host response during the course of primary pneumonic plague was investigated in two mouse strains, the outbred strain CD1 and the inbred strain C57BL/6. A comparative analysis of the course of disease in these two strains of mice indicated that they are susceptible to intranasal Y. pestis CO92 infection and have similar 50% lethal doses and kinetics of infection with respect to colonization of the lung, liver, and spleen. Significantly, in both strains of mice, robust neutrophil recruitment to the lungs was not observed until 48 h after infection, suggesting that there was a delay in inflammatory cell recruitment to the site of infection. In addition, proinflammatory cytokines (interleukin-6 [IL-6], tumor necrosis factor alpha, gamma interferon, IL-12p70, monocyte chemoattractant protein 1) and chemokines (KC, MIP-2) in the bronchoalveolar lavage fluids were not readily detected until 48 h after infection, which coincided with the increase in polymorphonuclear leukocyte (PMN) recruitment to the lungs. In comparison, CD1 mice with gram-negative pneumonia caused by Klebsiella pneumoniae exhibited strong inflammatory responses early in infection, with PMNs comprising the majority of the cells in the bronchoalveolar lavage fluid 24 h postinfection, indicating that PMN recruitment to the lungs could occur earlier in this infection than in Y. pestis infection. Together, our results indicate that there is a delay in the recruitment of neutrophils to the lungs in the mouse model of primary plague pneumonia that correlates with delayed expression of proinflammatory cytokines and chemokines in both outbred and inbred mice.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, The University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr., San Antonio, TX 78229. Phone: (210) 567-0657. Fax: (210) 567-6612. E-mail: dube{at}uthscsa.edu.

{triangledown} Published ahead of print on 13 November 2006.

Editor: J. B. Bliska

Infection and Immunity, February 2007, p. 697-705, Vol. 75, No. 2
0019-9567/07/$08.00+0     doi:10.1128/IAI.00403-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Ye, Z., Kerschen, E. J., Cohen, D. A., Kaplan, A. M., van Rooijen, N., Straley, S. C. (2009). Gr1+ Cells Control Growth of YopM-Negative Yersinia pestis during Systemic Plague. Infect. Immun. 77: 3791-3806 [Abstract] [Full Text]  
  • Thomas, R. J., Webber, D., Collinge, A., Stagg, A. J., Bailey, S. C., Nunez, A., Gates, A., Jayasekera, P. N., Taylor, R. R., Eley, S., Titball, R. W. (2009). Different Pathologies but Equal Levels of Responsiveness to the Recombinant F1 and V Antigen Vaccine and Ciprofloxacin in a Murine Model of Plague Caused by Small- and Large-Particle Aerosols. Infect. Immun. 77: 1315-1323 [Abstract] [Full Text]  
  • Lawrenz, M. B., Lenz, J. D., Miller, V. L. (2009). A Novel Autotransporter Adhesin Is Required for Efficient Colonization during Bubonic Plague. Infect. Immun. 77: 317-326 [Abstract] [Full Text]  
  • Agar, S. L., Sha, J., Foltz, S. M., Erova, T. E., Walberg, K. G., Parham, T. E., Baze, W. B., Suarez, G., Peterson, J. W., Chopra, A. K. (2008). Characterization of a mouse model of plague after aerosolization of Yersinia pestis CO92. Microbiology 154: 1939-1948 [Abstract] [Full Text]  
  • Mares, C. A., Ojeda, S. S., Morris, E. G., Li, Q., Teale, J. M. (2008). Initial Delay in the Immune Response to Francisella tularensis Is Followed by Hypercytokinemia Characteristic of Severe Sepsis and Correlating with Upregulation and Release of Damage-Associated Molecular Patterns. Infect. Immun. 76: 3001-3010 [Abstract] [Full Text]  
  • Bubeck, S. S., Dube, P. H. (2007). Yersinia pestis CO92{Delta}yopH Is a Potent Live, Attenuated Plague Vaccine. CVI 14: 1235-1238 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»