‘Division of labour’ in response to host oxidative burst drives a fatal Cryptococcus gattii outbreak

Kerstin Voelz, Simon A. Johnston, Leanne M. Smith, Rebecca A. Hall, Alexander Idnurm and Robin C. May ()
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Kerstin Voelz: Institute of Microbiology and Infection, School of Biosciences, University of Birmingham
Simon A. Johnston: University of Sheffield, Medical School
Leanne M. Smith: Institute of Microbiology and Infection, School of Biosciences, University of Birmingham
Rebecca A. Hall: Institute of Microbiology and Infection, School of Biosciences, University of Birmingham
Alexander Idnurm: School of Biological Sciences, University of Missouri
Robin C. May: Institute of Microbiology and Infection, School of Biosciences, University of Birmingham

Nature Communications, 2014, vol. 5, issue 1, 1-12

Abstract: Abstract Cryptococcus gattii is an emerging intracellular pathogen and the cause of the largest primary outbreak of a life-threatening fungal disease in a healthy population. Outbreak strains share a unique mitochondrial gene expression profile and an increased ability to tubularize their mitochondria within host macrophages. However, the underlying mechanism that causes this lineage of C. gattii to be virulent in immunocompetent individuals remains unexplained. Here we show that a subpopulation of intracellular C. gattii adopts a tubular mitochondrial morphology in response to host reactive oxygen species. These fungal cells then facilitate the rapid growth of neighbouring C. gattii cells with non-tubular mitochondria, allowing for effective establishment of the pathogen within a macrophage intracellular niche. Thus, host reactive oxygen species, an essential component of the innate immune response, act as major signalling molecules to trigger a ‘division of labour’ in the intracellular fungal population, leading to increased pathogenesis within this outbreak lineage.

Date: 2014
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DOI: 10.1038/ncomms6194

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