New research has yielded a greater understanding of how mucosal surfaces in the body respond to Candida albicans to prevent damage being done during infection.
The researchers, from King's College of London, presented their findings on September 3 at the Society for General Microbiology Autumn Conference.
The researchers focused on oral epithelial cells providing a barrier against microbes and challenged oral epithelial cells grown in vitro with C. albicans, which is known as an opportunistic pathogen that can colonize and infect individuals with a compromised immune system. They looked at gene expression six and 24 hours after infection.
The results showed that a molecular signaling pathway -- 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, the researchers noted. They found that 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. The researchers hope that by boosting the activity of the pathway it may be possible to reduce the fungus's ability to cause tissue damage.
Candida infections are the third most commonly acquired hospital blood-borne infection, resulting in 50,000 deaths annually in the U.K., according to the researchers.
