This Article Full Text Full Text (PDF) Other Versions of this Article: IAI.01287-06v1 75/1/429    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Fisher, M. L. Articles by Mecsas, J. Search for Related Content PubMed PubMed Citation Articles by Fisher, M. L. Articles by Mecsas, J.

 Previous Article  |  Next Article 

Infection and Immunity, January 2007, p. 429-442, Vol. 75, No. 1
0019-9567/07/$08.00+0     doi:10.1128/IAI.01287-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Intranasal Inoculation of Mice with Yersinia pseudotuberculosis Causes a Lethal Lung Infection That Is Dependent on Yersinia Outer Proteins and PhoP

Department of Microbiology and Molecular Biology, Tufts University, Boston, Massachusetts 02111

Received 10 August 2006/ Returned for modification 25 September 2006/ Accepted 13 October 2006

Yersinia pseudotuberculosis infects many mammals and birds including humans, livestock, and wild rodents and can be recovered from the lungs of infected animals. To determine the Y. pseudotuberculosis factors important for growth during lung infection, we developed an intranasal model of infection in mice. Following intranasal inoculation, we monitored both bacterial growth in lungs and dissemination to systemic tissues. Intranasal inoculation with as few as 18 CFU of Y. pseudotuberculosis caused a lethal lung infection in some mice. Over the course of 7 days, wild-type Y. pseudotuberculosis replicated to nearly 1 x 10⁸ CFU/g of lung in BALB/c mice, induced histopathology in lungs consistent with pneumonia, but disseminated sporadically to other tissues. In contrast, a yopB deletion strain was attenuated in this model, indicating that translocation of Yersinia outer proteins (Yops) is essential for virulence. Additionally, a yopH null mutant failed to grow to wild-type levels by 4 days postintranasal inoculation, but deletions of any other single effector YOP did not attenuate lung colonization 4 days postinfection. Strains with deletions in yopH and any one of the other known effector yop genes were more attenuated that the yopH strain, indicating a unique role for yopH in lungs. In summary, we have characterized the progression of a lung infection with an enteric Yersinia pathogen and shown that YopB and YopH are important in lung colonization and dissemination. Furthermore, this lung infection model with Y. pseudotuberculosis can be used to test potential therapeutics against Yersinia and other gram-negative infections in lungs.

Published ahead of print on 30 October 2006.

Editor: D. L. Burns

This article has been cited by other articles:

• Zhang, S., Zhang, Z., Liu, S., Bingham, W., Wilson, F. (2008). Fatal yersiniosis in farmed deer caused by Yersinia pseudotuberculosis serotype O:3 encoding a mannosyltransferase-like protein WbyK. jvdi 20: 356-359 [Abstract] [Full Text]  
• Auerbuch, V., Isberg, R. R. (2007). Growth of Yersinia pseudotuberculosis in Mice Occurs Independently of Toll-Like Receptor 2 Expression and Induction of Interleukin-10. Infect. Immun. 75: 3561-3570 [Abstract] [Full Text]