Background

Fungal colonizers of humans have evolved to sense and adapt to niches available in the host (Grahl and Cramer, 2010). Oxygen is a changing environmental parameter. Levels change in different tissues and during different stages of infection and immune activation (Carreau et al., 2011; Wenger et al., 2015). The ability to sustain growth and to survive in low oxygen environments has been linked to virulence in several fungi (Shepardson et al., 2013; Gresnigt et al., 2016; Pradhan et al., 2018). We have developed a protocol to follow the generation of hypoxia in a mouse infected with C. albicans (Lopes et al., 2018). We chose subdermal infection as a local, non-disseminated model of mycosis with acute onset which allows analysis of hypoxia in a confined space, where C. albicans and host cells interact (Urban et al., 2009; Santus et al., 2018). Thereby, natural variation of oxygen levels in other tissues can be eliminated and secondary effects from distant locations arising in systemic infection can be avoided. During infection, hypoxia is created mainly by neutrophil influx to the site of infection. Neutrophil extravasation and the activation of oxygen-consuming enzymes create environments with low oxygen levels. In turn, C. albicans exploits this environmental shift to avoid immune recognition by changing cell wall composition leading to masking of recognized entities (Lopes et al., 2018).