The fungus Candida auris, responsible for sometimes serious infections in hospitals, has a particularly effective hiding place: hair follicles.
Experiments show that it can persist there for a long time by taking advantage of a reaction from our own immune system. This behavior helps explain why it remains so difficult to eliminate from the skin.
Yet the skin is an effective defensive barrier. When a microbe settles there, immune cells trigger reactions intended to eliminate it. With Candida auris, this response does not produce the expected effect.
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To understand this phenomenon, scientists compared Candida auris with Candida albicans, a related yeast that is much more familiar to the human body. In mice, C. albicans quickly disappeared after being deposited on the skin. C. auris, by contrast, remained detectable for up to 30 days and was frequently found around hairs and inside their follicles.
The fungus also adheres directly to human hair during laboratory experiments. This ability appears to facilitate its access to follicles, the small cavities in the skin where hairs grow.
The difference is notably due to the immune response that is triggered. In response to C. albicans, the body produces a response that strengthens the skin's antifungal defenses. C. auris causes greater production of interferon gamma, a molecule used by immune cells to communicate and organize certain defenses.
Here, this reaction paradoxically benefits the fungus. Interferon gamma acts on keratinocytes, the cells that form a large part of the skin's protective layer. In colonized follicles, several defense mechanisms against fungi and mechanisms that maintain this barrier become less active.
The experiments confirm this link. When mouse skin cells could no longer receive the interferon gamma signal, the amount of Candida auris present decreased. Conversely, high production of this molecule favored its presence. The microbe therefore does more than resist immunity: the reaction it triggers helps make its refuge more welcoming.
This persistence is particularly significant in healthcare facilities. Candida auris can colonize a person without immediately causing illness and then spread. Some strains resist several antifungal treatments, which subsequently complicates the management of an invasive infection.
The next step is to determine how to prevent this long-term colonization without disrupting the skin's normal defenses. The mechanisms observed around interferon gamma and the follicles provide precise targets for studying new strategies against colonization, even before a deep infection occurs.