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Infection and Immunity, May 2007, p. 2143-2151, Vol. 75, No. 5
0019-9567/07/$08.00+0     doi:10.1128/IAI.01680-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Niche-Specific Activation of the Oxidative Stress Response by the Pathogenic Fungus Candida albicans{triangledown}

Brice Enjalbert, Donna M. MacCallum, Frank C. Odds, and Alistair J. P. Brown*

Aberdeen Fungal Group, School of Medical Sciences, Institute of Medical Sciences, University of Aberdeen, Aberdeen AB25 2ZD, United Kingdom

Received 20 October 2006/ Returned for modification 23 November 2006/ Accepted 22 February 2007

Candida albicans is a major opportunistic pathogen of humans. The pathogenicity of this fungus depends upon its ability to deal effectively with the host defenses and, in particular, the oxidative burst of phagocytic cells. We have explored the activation of the oxidative stress response in C. albicans in ex vivo infection models and during systemic infection of a mammalian host. We have generated C. albicans strains that contain specific green fluorescent protein (GFP) promoter fusions and hence act as biosensors of environmental oxidative stress at the single-cell level. Having confirmed that CTA1-, TRX1-, and TTR1/GRX2-GFP reporters respond specifically to oxidative stress, and not to heat shock, nitrosative, or osmotic stresses, we used these reporters to show that individual C. albicans cells activate an oxidative stress response following phagocytosis by neutrophils, but not by macrophages. Significantly, only a small proportion of C. albicans cells (about 4%) activated an oxidative stress response during systemic infection of the mouse kidney. The response of these cells was generally equivalent to exposure to 0.4 mM hydrogen peroxide in vitro. We conclude that most C. albicans cells are exposed to an oxidative stress when they come into contact with neutrophils in the bloodstream of the host but that oxidative killing is no longer a significant threat once an infection has been established in the kidney.

* Corresponding author. Mailing address: Aberdeen Fungal Group, School of Medical Sciences, Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen AB25 2ZD, United Kingdom. Phone: 44-1224-555883. Fax: 44-1224-555844. E-mail: al.brown{at}abdn.ac.uk

{triangledown} Published ahead of print on 5 March 2007.

Editor: A. Casadevall

Infection and Immunity, May 2007, p. 2143-2151, Vol. 75, No. 5
0019-9567/07/$08.00+0     doi:10.1128/IAI.01680-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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