Candida albicans is the most common species of the candida fungus and is the leading cause of vaginal and oral yeast infections, including thrush and denture stomatitis. It is the fourth most common hospital-acquired-blood-borne pathogen in the United States and surprisingly, it is present in the mouths of 30–50% of healthy adults.

Because of the widespread nature of candida, the potential for overgrowth and infection is common in the young, elderly, immuno-compromised and people receiving corticosteroid or chemotherapy treatments.
The findings, published in Cell, Host and Microbe, identified the critical role of a protein, interleukin-1β or IL-1β, secreted by a variety of cells in the human immune system to protect the body from oral colonisation by candida albicans and preventing it from spreading to infect host tissue and blood. The study defines the precise mechanism by which the body's immune cells produce IL-1β following contact with candida albicans. Further, it shows that a complex of proteins, collectively termed the NLRP3 inflammasome, function to produce IL-1β from an inactive, precursor form into a form that can be secreted by cells and subsequently function to modulate the immune system and its responses.

This research clarifies a number of mechanisms and pathways that may be therapeutic targets to help alleviate and/or eliminate Candida overgrowth and its accompanying symptoms, such as pain and discomfort, swelling, burning sensation of affected area and difficulty swallowing in individuals suffering from infections.
The findings of a team of researchers led by Amy Hise, assistant professor at the Center for Global Health and Diseases, Case Western Reserve University School of Medicine, will open many new avenues of research in fungal infections. One direction they are pursuing is to identify the way that the fungus activates the inflammasome. This might provide new targets for drug development. Another area of interest is the investigation of how small differences between individuals in immune related genes, called single nucleotide polymorphisms or SNPs, affect susceptibility to fungal and other infections.

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First Published in September 2009

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