Dr. Glen Palmer, Assistant Professor of Microbiology, Immunology & Parasitology at Louisiana State University (LSU) Health Sciences Center New Orleans, was part of an international research team led by Dr. Luigina Romani, at the University of Perugia in Italy, that discovered opportunistic fungi like Candida albicans can sense the immune status of host cells and adapt, evading immune system defenses. Unlike previous studies, this research investigated both sides of the infection equation, as well as the interaction between the fungi and the cells they will invade. The findings were published online on February 21, 2012 in Nature Communications. This study demonstrates that this process is much more elaborate and complex than previously understood. The researchers determined that C. albicans binds to the host immune signaling molecule, interleukin (IL) 17A, which permits the fungus to navigate and tolerate the active immune environment of healthy host tissue, mounting effective countermeasures. IL-17A may also contribute to disease susceptibility by modifying the intrinsic virulence of the fungus. This study provides molecular evidence that by exploiting IL-17A, the fungus not only survives, but can cause disease to develop. "It's a bit like the fungus is listening in to the conversations our immune system is having so it can best determine how to react and survive in our tissues. This may also be a crucial step in determining when this opportunist decides to invade host tissue and cause life-threatening disease in an immunosuppressed patient," notes Dr. Palmer. According to the Centers for Disease Control and Prevention, there are more than 20 species of Candida yeasts that can cause infection in humans, the most common of which is Candida albicans.
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