Scientists Discover How Deadly Fungi Weaken the Immune System; Open Door to New Treatments

by AHT Desk

Researchers at the University of Sheffield in London have identified a mechanism by which dangerous fungi evade the body's immune defences, a breakthrough that could pave the way for new therapies against life-threatening fungal infections and growing antifungal drug resistance, especially among individuals with weakened immune system.

The study found that Candida albicans—a common fungus that normally lives harmlessly in many healthy people—can suppress a key immune response used by neutrophils, the white blood cells that form the body's first line of defence against infections. By reducing the production of reactive nitrogen species (RNS), toxic molecules that help destroy invading microbes, the fungus effectively weakens the immune system's ability to eliminate the infection.

Although Candida albicans is part of the normal microbial community in an estimated 40 to 60 per cent of healthy individuals, it can become dangerous in people with weakened immune systems. Once it enters the bloodstream, it can cause invasive candidiasis, a severe infection associated with high mortality rates.

Using zebrafish models and human immune cells, researchers demonstrated that restoring the suppressed immune response significantly improved survival rates. The benefits were even greater when immune restoration was combined with existing antifungal medications, suggesting that strengthening the body's own defences could enhance the effectiveness of current treatments.

The research also showed that other clinically important fungal pathogens, including the multidrug-resistant Candida auris, employ similar immune-suppressing strategies. Both Candida albicans and Candida auris have been identified by the World Health Organization as priority fungal pathogens because of increasing drug resistance and the limited availability of effective therapies.

Scientists observed that fungal strains capable of suppressing neutrophil activity more effectively caused more severe infections in laboratory models. The findings suggest that disabling the host immune response is a major factor contributing to fungal virulence.

Researchers believe the discovery could accelerate the development of host-directed therapies—treatments designed to boost the patient's immune response rather than directly targeting the fungus. Such approaches may become increasingly valuable as resistance to antifungal drugs continues to rise globally.

The team plans to investigate the precise biological mechanisms that allow Candida to interfere with neutrophil function and assess whether therapies aimed at restoring reactive nitrogen species can eventually be used alongside conventional antifungal drugs in clinical settings.