New findings on the fungus which causes thrush have helped explain how it evades destruction by the immune system, according to Scottish researchers.
Candida albicans does not produce the usual antigens on its cell surface, which would normally stimulate the innate immune response. This is a particular problem as C. albicans can represent a serious threat for immunocompromised people, such as cancer or transplant patients.
A team from Aberdeen University, UK, carried out lab tests and found that C. albicans avoids immune detection by presenting "a moving immunological target".
They write in Monday’s Nature Microbiology that: "Beta-glucan, a key pathogen-associated molecular pattern 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 beta-glucan, masking in C. albicans via a signalling pathway, in a process that reduces the visibility of the fungus to the immune system."
Professor Al Brown, who led the research, says: "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. The fungus is playing a deadly game of hide-and-seek.
"Whilst for many healthy individuals C. 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 favour of the patient.
"We are now starting to define how these discoveries, which were made under well-defined laboratory conditions, relate to infections in real patients."
Ballou, E. R. et al. Lactate signalling regulates fungal beta-glucan masking and immune evasion. Nature Microbiology 12 December 2016; doi:10.1038/nmicrobiol.2016.238 [abstract]
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