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 Torosantucci, A.
Right arrow Articles by Calderone, R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Torosantucci, A.
Right arrow Articles by Calderone, R.

 Previous Article  |  Next Article 

Infection and Immunity, February 2002, p. 985-987, Vol. 70, No. 2
0019-9567/01/$04.00+0     DOI: 70.2.985-987.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Deletion of the Two-Component Histidine Kinase Gene (CHK1) of Candida albicans Contributes to Enhanced Growth Inhibition and Killing by Human Neutrophils In Vitro

Antonella Torosantucci,1 Paola Chiani,1 Flavia De Bernardis,1 Antonio Cassone,1 Jose Antonio Calera,2 and Richard Calderone3*

Istituto Superiore di Sanita, Laboratory of Bacteriology and Mycology, Viale Regina Elena 299, Rome 00196, Italy,1 Department of MicrobiologyImmunology, Georgetown University Medical Center, Washington, D.C. ,3 Departamento de Microbiologia y Genetica, Universidad de Salamanca, Salamanca, Spain2

Received 18 July 2001/ Returned for modification 30 August 2001/ Accepted 8 November 2001

We have observed that human neutrophils (polymorphonuclear leukocytes [PMNs]) have an increased growth-inhibitory and killing effect on a strain of Candida albicans with a deletion of CHK1, a gene encoding a putative histidine kinase. The PMN effect was not due to increased phagocytosis of the null strain. This observation may partially explain the reduced virulence in a hematogenously disseminated murine model of candidiasis.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, Georgetown University Medical Center, 312 SE Med-Dent Building, 3900 Reservoir Rd., NW, Washington, DC 20007-2197. Phone: (202) 687-1137. Fax: (202) 687-1800. E-mail: calderor{at}georgetown.edu.

Editor: T. R. Kozel

Infection and Immunity, February 2002, p. 985-987, Vol. 70, No. 2
0019-9567/01/$04.00+0     DOI: 70.2.985-987.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Chauhan, N., Calderone, R. (2008). Two-Component Signal Transduction Proteins as Potential Drug Targets in Medically Important Fungi. Infect. Immun. 76: 4795-4803 [Full Text]  
  • Cheetham, J., Smith, D. A., da Silva Dantas, A., Doris, K. S., Patterson, M. J., Bruce, C. R., Quinn, J. (2007). A Single MAPKKK Regulates the Hog1 MAPK Pathway in the Pathogenic Fungus Candida albicans. Mol. Biol. Cell 18: 4603-4614 [Abstract] [Full Text]  
  • Li, D., Gurkovska, V., Sheridan, M., Calderone, R., Chauhan, N. (2004). Studies on the regulation of the two-component histidine kinase gene CHK1 in Candida albicans using the heterologous lacZ reporter gene. Microbiology 150: 3305-3313 [Abstract] [Full Text]  
  • Marcil, A., Harcus, D., Thomas, D. Y., Whiteway, M. (2002). Candida albicans Killing by RAW 264.7 Mouse Macrophage Cells: Effects of Candida Genotype, Infection Ratios, and Gamma Interferon Treatment. Infect. Immun. 70: 6319-6329 [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»