Interaction of the mucosal barrier with accessory immune cells during fungal infection.

The mucosal epithelium is of central importance in host defence and immune surveillance, as it is the primary cell layer that initially encounters environmental microorganisms. Induction of antifungal innate immune responses depends on recognition of fungal components by host pattern recognition receptors. Members of the Toll-like receptor family have emerged as key sensors that recognize fungal pathogens and trigger defence responses. During oral infection with the fungal pathogen Candida albicans, a large number of cytokines is secreted by oral epithelial cells, which in turn activate myeloid cells in the submucosal layers to clear the invading pathogen. Recent data provide novel insights into the complex molecular mechanisms of innate immune responses initiated by cooperation between epithelial cells and neutrophils. In this review, we discuss the role of epithelial TLRs and how the immunological crosstalk between C. albicans-infected oral epithelium and neutrophils protects the mucosal surface from fungal invasion and cell injury.