Sensing of mammalian IL-17A regulates fungal adaptation and virulence

• Published in: Nature communications 2012-02, Vol.3 (1), p.683-683, Article 683
• Main Authors: Zelante, Teresa, Iannitti, Rossana G., De Luca, Antonella, Arroyo, Javier, Blanco, Noelia, Servillo, Giuseppe, Sanglard, Dominique, Reichard, Utz, Palmer, Glen E., Latgè, Jean-Paul, Puccetti, Paolo, Romani, Luigina
• Format: Article
• Language: English
• Subjects: 631/250/127/1213; 631/326/193/2542; 692/699/255/1672; Adaptation; Adaptation, Physiological; Animals; Aspergillus fumigatus - immunology; Aspergillus fumigatus - pathogenicity; Aspergillus fumigatus - physiology; Autophagy; Candida albicans - immunology; Candida albicans - pathogenicity; Candida albicans - physiology; Cyclic AMP - biosynthesis; Cytokines; Female; Gene Expression Profiling; Genomes; Host-Pathogen Interactions; Humanities and Social Sciences; Infections; Interleukin-17 - metabolism; Metabolism; Mice; Mice, Inbred C57BL; Morphology; multidisciplinary; Pathogens; Scanning electron microscopy; Science; Science (multidisciplinary); Signal Transduction; TOR Serine-Threonine Kinases - metabolism; Virulence
• ISSN: 2041-1723; 2041-1723
• DOI: 10.1038/ncomms1685

Infections by opportunistic fungi have traditionally been viewed as the gross result of a pathogenic automatism, which makes a weakened host more vulnerable to microbial insults. However, fungal sensing of a host's immune environment might render this process more elaborate than previously appreciated. Here we show that interleukin (IL)-17A binds fungal cells, thus tackling both sides of the host–pathogen interaction in experimental settings of host colonization and/or chronic infection. Global transcriptional profiling reveals that IL-17A induces artificial nutrient starvation conditions in Candida albicans , resulting in a downregulation of the target of rapamycin signalling pathway and in an increase in autophagic responses and intracellular cAMP. The augmented adhesion and filamentous growth, also observed with Aspergillus fumigatus , eventually translates into enhanced biofilm formation and resistance to local antifungal defenses. This might exemplify a mechanism whereby fungi have evolved a means of sensing host immunity to ensure their own persistence in an immunologically dynamic environment. It is unclear whether pathogens can advantageously exploit the host's immune response. Using Candida albicans , the authors show that host IL-17A binds to the fungi and induces nutrient starvation and autophagy, which eventually leads to enhanced biofilm formation and resistance to the hosts' defence.