ABSTRACT
The attachment of fungi to epithelial cells appears to occur through lectin-, laminin-, and fibronectinlvitronectin-mediated binding to complementary receptors on epithelial surfaces, and does not necessarily disrupt the metabolic, structural, or barrier function of epithelia [3,4,9,10]. Inversely, a number of important mediators, including defensins, chemokines, and cytokines, are released upon epithelial cell encounter with fungi [12-14J. These findings suggest that the epithelial cells are crucially involved in orchestration of the subsequent inflammatory and immunological responses to fungi. In addition, epithelial cells themselves may be endowed with some antifungal effector activities, as shown by the ability of epithelial cells from the vagina
to inhibit C. albicans growth ([1] and references therein) and of those from lungs to internalize A. fumigatus conidia [15]. However, internalization of Aspergillus conidia by type II pneumocytes may not prevent hyphal formation, suggesting that in pulmonary defense mechanisms against filamentous fungi, epithelial cells do not participate in the host control of conidial germination and hyphal growth.
