Previous Article | Next Article ![]()
Infection and Immunity, August 2004, p. 4878-4880, Vol. 72, No. 8
0019-9567/04/$08.00+0 DOI: 10.1128/IAI.72.8.4878-4880.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
Rachana Parmar,1 Marife Espiritu,1 and David A. Stevens1,2,3
California Institute for Medical Research,1 Department of Medicine, Division of Infectious Diseases, Santa Clara Valley Medical Center, San Jose, California 95128,2 Department of Medicine, Division of Infectious Diseases and Geographic Medicine, Stanford University, Stanford, California 94305,3 Section on Neurobiology, Physiology and Behavior, University of California, Davis, California 956164
Received 16 January 2004/ Returned for modification 1 March 2004/ Accepted 3 May 2004
We compared susceptibility to Candida vaginitis in derived murine substrains differing in sensitivity to estrogen (CD-1 and CD10, resistant; CD3 and C57BL/6 responsive), and in F1 crosses. The order of decreasing resistance was CD-1
CD10
CD10 x CD3F1 > CD10 x B6F1 > CD3 > C57BL/6 and correlated with estrogen responsiveness in endocrine disruptor assays. Resistance to Candida vaginitis appears additive in CD10 x B6F1 animals and dominant in CD10 x CD3F1 animals.
Present address: Department of Environmental Toxicology, University of California, Davis, CA 95616.
This article has been cited by other articles:
| J. Bacteriol. | J. Virol. | Eukaryot. Cell |
|---|
| Microbiol. Mol. Biol. Rev. | Clin. Vaccine Immunol. | All ASM Journals |
|---|