Candida albicans is a common fungus found living in, and on, many parts of the human body. Usually this species causes no harm to humans unless it can breach the body's immune defences, where can lead to serious illness or death. It is known as an opportunistic pathogen that can colonise and infect individuals with a compromised immune system. New research, presented today at the Society for General Microbiology's Autumn Conference, gives us a greater understanding of how mucosal surfaces in the body respond to C. albicans to prevent damage being done during infection.
Researchers from King's College London focused on oral epithelial cells, a mucosal layer of cells that line the mouth, providing a barrier against microbes. The group challenged oral epithelial cells grown in vitro with C. albicans, looking at gene expression six and 24 hours after infection.
The results showed that a molecular signalling pathway know as the 'PI3 Kinase pathway' is activated as soon as five minutes after the epithelial cells encounter C. albicans, before the fungus has time to become invasive. This pathway seems to be involved in priming epithelial cells to protect against future damage. Inhibiting the PI3 Kinase pathway increased the amount of damage caused by C. albicans and reduced the normal tissue healing response.
This finding makes the PI3 Kinase pathway an attractive target for new therapeutics against C. albicans. Dr David Moyes, who presented the work at the conference, hopes that by boosting the activity of the pathway it may be possible to reduce the fungus's ability to cause tissue damage.