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 Pal, S.
Right arrow Articles by de la Maza, L. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Pal, S.
Right arrow Articles by de la Maza, L. M.

 Previous Article  |  Next Article 

Infection and Immunity, August 2000, p. 4831-4833, Vol. 68, No. 8
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Role of Nramp1 Deletion in Chlamydia Infection in Mice

Sukumar Pal, Ellena M. Peterson, and Luis M. de la Maza*

Department of Pathology, University of California, Irvine, Irvine, California, 92697-4800

Received 1 March 2000/Returned for modification 27 April 2000/Accepted 11 May 2000

Elicited macrophages from 129sv mice with a functional deletion of the natural-resistance-associated macrophage protein 1 gene (Nramp1) were shown to be as susceptible as wild-type mice to infection with the Chlamydia trachomatis mouse pneumonitis and L3 serovars and to Chlamydia pneumoniae. Furthermore, the two groups of mice were shown to be similarly susceptible to an intranasal infection with these microorganisms. In conclusion, the Nramp1 gene does not appear to play a major role in the regulation of the susceptibility of mice to a chlamydial infection.

* Corresponding author. Mailing address: Department of Pathology, Medical Sciences I, Room D440, University of California, Irvine, Irvine, CA 92697-4800. Phone: (949) 824-7450. Fax: (949) 824-2160. E-mail: lmdelama{at}uci.edu.

Infection and Immunity, August 2000, p. 4831-4833, Vol. 68, No. 8
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:

  • de Kruif, M. D., van Gorp, E. C.M., Keller, T. T., Ossewaarde, J. M., ten Cate, H. (2005). Chlamydia pneumoniae infections in mouse models: relevance for atherosclerosis research. Cardiovasc Res 65: 317-327 [Abstract] [Full Text]  
  • Guilloteau, L. A., Dornand, J., Gross, A., Olivier, M., Cortade, F., Vern, Y. L., Kerboeuf, D. (2003). Nramp1 Is Not a Major Determinant in the Control of Brucella melitensis Infection in Mice. Infect. Immun. 71: 621-628 [Abstract] [Full Text]  
  • Morrison, R. P., Caldwell, H. D. (2002). Immunity to Murine Chlamydial Genital Infection. Infect. Immun. 70: 2741-2751 [Full Text]  
  • Gigliotti Rothfuchs, A., Gigliotti, D., Palmblad, K., Andersson, U., Wigzell, H., Rottenberg, M. E. (2001). IFN-{alpha}{beta}-Dependent, IFN-{gamma} Secretion by Bone Marrow-Derived Macrophages Controls an Intracellular Bacterial Infection. J. Immunol. 167: 6453-6461 [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»