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 Google Scholar
Google Scholar
Right arrow Articles by Turner, J. K.
Right arrow Articles by Tapping, R. I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Turner, J. K.
Right arrow Articles by Tapping, R. I.

 Previous Article  |  Next Article 

Infection and Immunity, September 2008, p. 4092-4099, Vol. 76, No. 9
0019-9567/08/$08.00+0     doi:10.1128/IAI.00488-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

The Resistance of BALB/cJ Mice to Yersinia pestis Maps to the Major Histocompatibility Complex of Chromosome 17{triangledown}

Joshua K. Turner,1 Milton M. McAllister,3 John L. Xu,1 and Richard I. Tapping1,2*

Department of Microbiology,1 College of Medicine,2 College of Veterinary Medicine, University of Illinois at Urbana-Champaign, Urbana, Illinois 618013

Received 19 April 2008/ Returned for modification 11 June 2008/ Accepted 14 June 2008

Yersinia pestis, the causative agent of plague, has been well studied at the molecular and genetic levels, but little is known about the role that host genes play in combating this highly lethal pathogen. We challenged several inbred strains of mice with Y. pestis and found that BALB/cJ mice are highly resistant compared to susceptible strains such as C57BL/6J. This resistance was observed only in BALB/cJ mice and not in other BALB/c substrains. Compared to C57BL/6J mice, the BALB/cJ strain exhibited reduced bacterial burden in the spleen and liver early after infection as well as lower levels of serum interleukin-6. These differences were evident 24 h postinfection and became more pronounced with time. Although a significant influx of neutrophils in the spleen and liver was exhibited in both strains, occlusive fibrinous thrombi resulting in necrosis of the surrounding tissue was observed only in C57BL/6J mice. In an effort to identify the gene(s) responsible for resistance, we measured total splenic bacteria in 95 F2 mice 48 h postinfection and performed quantitative trait locus mapping using 58 microsatellite markers spaced throughout the genome. This analysis revealed a single nonrecessive plague resistance locus, designated prl1 (plague resistance locus 1), which coincides with the major histocompatibility complex of chromosome 17. A second screen of 95 backcrossed mice verified that this locus confers resistance to Y. pestis early in infection. Finally, eighth generation backcrossed mice harboring prl1 were found to maintain resistance in the susceptible C57BL/6J background. These results identify a novel genetic locus in BALB/cJ mice that confers resistance to Y. pestis.

* Corresponding author. Mailing address: Department of Microbiology, B103 Chemical and Life Science Building, MC 110, University of Illinois at Urbana-Champaign, 601 South Goodwin Avenue, Urbana, IL 61801. Phone: (217) 244-7940. Fax: (217) 244-6697. E-mail:tapping{at}life.uiuc.edu

{triangledown} Published ahead of print on 23 June 2008.

Editor: J. B. Bliska

Infection and Immunity, September 2008, p. 4092-4099, Vol. 76, No. 9
0019-9567/08/$08.00+0     doi:10.1128/IAI.00488-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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