The opportunistic fungal pathogen Candida albicans（白色念珠菌） inconspicuously（难以觉察地） lives in our bodies until it senses that we are weak, when it quickly adapts to go on the offensive. The fungus1, known for causing yeast2 and other minor3 infections, also causes a sometimes-fatal infection known as candidemia（念珠菌血症） in immunocompromised patients. An in vivo study, published in mBio, demonstrates how C. albicans can distinguish between a healthy and an unhealthy host and alter its physiology4（生理机能） to attack. "The ability of the fungus to sense the immune status of its host may be key to its ability to colonize5 harmlessly in some people but become a deadly pathogen in others," said Jessica V. Pierce, BA, PhD student in the molecular6 microbiology program at the Sackler School of Graduate Biomedical Sciences at Tufts.
"Effective detection and treatment of disease in immunocompromised patients could potentially work by targeting the levels of a protein, Efg1p, that we found influenced the growth of Candida albicans inside the host," she continued.
The researchers knew from previous research that Efg1p influences the expression of
genes7 that regulate how harmful a fungal cell can become. Surprisingly, the
investigators8 found that lower Efg1p levels allow the fungal cells to grow to high levels inside a host. Higher levels of the protein result in less growth.
To examine how the immune status could affect the growth of C. albicans within a host, the researchers fed both healthy and immunocompromised mice equal amounts of two fungal strains containing two different levels of the Efg1p protein.
Fecal pellets from the mice were tested to determine which strain of
fungi9 thrived. In a healthy host, the fungal cells with higher levels of the protein predominated.
In immunocompromised mice, the fungal cells with lower levels of the protein flourished. The researchers
noted10 that lack of interactions with immune cells in the
intestinal11 tract12 most likely caused the necessary environmental conditions favoring fungal cells that express lower levels of the protein, resulting in fungal overgrowth and setting the stage for systemic infection.
"By having a mixed population with some high Efg1p cells and some low Efg1p cells, the fungus can adjust its physiology to remain
benign13 or become harmful when it
colonizes14 hosts with varying immune statuses. These findings are important because they provide the first steps toward developing more effective methods for detecting and treating serious and stubborn infections caused by Candida albicans, such as candidemia," said Carol A. Kumamoto, PhD, professor of molecular biology and microbiology at Tufts University School of Medicine and member of the molecular microbiology and genetics program
faculties15 at the Sackler School of Graduate Biomedical Sciences.
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