Candida albicans is a pathogenic yeast commonly found in the intestinal digestive tract of healthy individuals. Candida albicans is usually limited to the intestines of the digestive tract, where it causes harmless commensal colonization. However, Candida albicans can also infect various parts of the body such as the skin, nails, mouth, vagina, airways and bloodstream, causing both superficial and disseminated infections. Candidiasis refers to chronic infections by Candida albicans. Candidiasis is often fatal among patients with compromised immune system such as organ and bone marrow transplant recipients, human immunodeficiency virus carriers, and neonates. Candidiasis has become more common due to its increasing incidence in immunocompromised patients (5-10) and its development of resistance toward the limited range of available antifungal agents (11-15).
Diagnostic kits for the detection of commensal colonization by Candida albicans in humans are currently available. However, as approximately 60% of healthy individuals harbor Candida albicans in their gastrointestinal tract, it is important to identify specific marker genes which can differentiate a harmless commensal colonization from a life-threatening blood-borne disseminated infection.
Recently, hemoglobin, a component of blood, has been identified as a host factor that specifically induces increased adhesion of C. albicans blastoconidia to fibronectin (20, 21). Fibronectin is a major component of the host extracellular matrix that may play an important role in the initiation and dissemination of C. albicans infection. Hemoglobin has also been shown to induce changes in expression of several proteins exposed on the yeast cell wall, including a 55 kDa protein that binds fibronectin (21, 22). Thus, the identification and characterization of hemoglobin-response genes may be useful in differentiating a harmless commensal colonization from a life-threatening blood-borne disseminated infection.
Recognition of host factors by pathogens may also initiate adaptive responses that facilitate infection. Successful pathogens have developed bidirectional signal transduction pathways to achieve environments in their hosts that are optimal for colonization and growth of the invading microorganisms (1-3). Following contact with the host, pathogens produce factors that alter gene expression or function in host cells to facilitate infection (2). Conversely, pathogenic microorganisms must also alter their gene expression in response to specific signals from the host (1, 3, 4). Thus, identification of host factor-response genes could lead to new therapeutic approaches to prevent or treat these infections.