Key Points
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This review provides an analysis of the signal transduction pathways that contribute to oxidant-stress adaptation in Candida albicans and Aspergillus fumigatus.
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In addition to the signal pathways, downstream effector proteins and their activities in oxidant neutralization are discussed.
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An analysis especially of the two-component signal transduction proteins and the relationship of these proteins to the Hog1p MAPK are discussed including differences among the two-component eukaryotic and prokaryotic proteins.
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The relationship of in vitro analysis of oxidant adaptation is extended in this review to a discussion of survival of pathogens in phagocytic cells.
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The neutrophil is the primary response cell in protection. Comparisons are made between PMNs and monocytes in their interactions with C. albicans.
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The pathogenesis of candidiasis and invasive aspergillosis is presented, and the early events in these processes are discussed in relationship to phagocyte functions.
Abstract
Candida species and Aspergillus fumigatus were once thought to be relatively benign organisms. However, it is now known that this is not the case ? Candida species rank among the top four causes of nosocomial infectious diseases in humans and A. fumigatus is the most deadly mould, often having a 90% mortality rate in immunocompromised transplant recipients. Adaptation to stress, including oxidative stress, is a necessary requisite for survival of these organisms during infection. Here, we describe the latest information on the signalling pathways and target proteins that contribute to oxidant adaptation in C. albicans and A. fumigatus, which has been obtained primarily through the analysis of mutants or inference from genome annotation.
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Some of the data included were supported by NIH-NIAID grants to R.C. and by an NIH-Fogarty International award to R.C. and J.-P.
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Chauhan, N., Latge, JP. & Calderone, R. Signalling and oxidant adaptation in Candida albicans and Aspergillus fumigatus. Nat Rev Microbiol 4, 435–444 (2006). https://doi.org/10.1038/nrmicro1426
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DOI: https://doi.org/10.1038/nrmicro1426
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