Abstract
Interactions between colonizing commensal microorganisms and their hosts play important roles in health and disease. The opportunistic fungal pathogen Candida albicans is a common component of human intestinal flora. To gain insight into C. albicans colonization, genes expressed by fungi grown within a host were studied. The EFH1 gene, encoding a putative transcription factor, was highly expressed during growth of C. albicans in the intestinal tract. Counterintuitively, an efh1 null mutant exhibited increased colonization of the murine intestinal tract, a model of commensal colonization, whereas an EFH1 overexpressing strain exhibited reduced colonization of the intestinal tract and of the oral cavity of athymic mice, the latter situation modeling human mucosal candidiasis. When inoculated into the bloodstream of mice, both efh1 null and EFH1 overexpressing strains caused lethal infections. In contrast, other mutants are attenuated in virulence following intravenous inoculation but exhibited normal levels of intestinal colonization. Finally, although expression of several genes is dependent on transcription factor Efg1p during laboratory growth, Efg1p-independent expression of these genes was observed during growth within the murine intestinal tract. These results show that expression of EFH1 regulated the level of colonizing fungi, favoring commensalism as opposed to candidiasis. Also, different genes are required in different host niches and the pathway(s) that regulates gene expression during host colonization can differ from well-characterized pathways used during laboratory growth.
Highlights
The opportunistic fungal pathogen Candida albicans colonizes its host long before disease arises
The studies described here analyze C. albicans cells colonizing the intestinal tract of immunocompetent mice in the absence of disease, a model for commensalism
Results showed that expression of the putative transcription factor Efh1p by cells colonizing the intestinal tract was relatively high, but paradoxically, expression of Efh1p was associated with lower colonization
Summary
The opportunistic fungal pathogen Candida albicans colonizes its host long before disease arises. C. albicans colonization of the oral cavity is detected in most infants by the age of one month [1]. The majority of adults are detectably colonized in the intestinal tract by C. albicans [2]. Colonization is believed to persist for long periods of time [2], and in this situation, C. albicans is primarily nonpathogenic. If the host becomes immunocompromised, disease caused by dissemination of commensal organisms from the intestinal tract can occur. Disseminated candidiasis occurs in neutropenic patients, and Candida spp are among the most common organisms isolated from the blood of hospitalized patients [3]. Despite the importance of commensal organisms as the source of infection, little is known about C. albicans factors that influence intestinal colonization
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