The mechanism by which the fungus that causes thrush attempts to hide from our body’s defenses, has been found by scientists from the University of Aberdeen.
The Candida albicans fungus lives in most of us and is relatively harmless most of the time. It is also a common cause of thrush.
But Candida can take hold and cause conditions such as thrush in babies, or the yeast infections that many women suffer after antibiotic treatments. If our defenses become weakened, as can happen in cancer or transplant patients, the fungus can be deadly.
Researchers from the University of Aberdeen’s world-leading Aberdeen Fungal Group and Medical Research Council Centre for Medical Mycology have revealed ways in which the fungus can ‘hide’ from our immune system.
Cell Surface Changes
Our body’s immune system normally detects the fungus by interacting with specific molecules on its cell surface and then kills the fungal invader. Meanwhile, when the fungus senses the lactic acid we produce as part of a normal, healthy lifestyle, it changes its cell surface to make it more difficult for our immune system to detect and kill it.
The work, led by Professor Al Brown from the Aberdeen Fungal Group, identifies the mechanisms that help the fungus mask itself from our immune detection system.
“We’ve discovered that this fungus is a moving target for our immune defences. It is very good at adapting to the environments within us and, through evolution, it has developed new ways to avoid being detected by our defences, said Professor Brown. “The fungus is playing a deadly game of hide-and-seek.
Whilst for many healthy individuals Candida albicans is not a problem, and thrush infections are generally straightforward to treat, Candida can be a major health concern for some hospitalised patients. So it is important to work out how this fungus survives inside us so that we can develop ways to tip the balance back in favor of the patient.”
In particular, the authors say in their abstract:
“We report that the exposure of β-glucan, a key pathogen-associated molecular pattern (PAMP) located at the cell surface of C. albicans and other pathogenic Candida species, is modulated in response to changes in the carbon source. Exposure to lactate induces β-glucan masking in C. albicans via a signalling pathway that has recruited an evolutionarily conserved receptor (Gpr1) and transcriptional factor (Crz1) from other well-characterized pathways. In response to lactate, these regulators control the expression of cell-wall-related genes that contribute to β-glucan masking.”