Figure 2.

Fungal–host interactions during fungal diseases that are mimicked by in vitro infection models discussed in this review. (A) Fungal–monocyte/macrophage interactions resulting in several effector mechanisms that contribute to immunity against fungal infections (ROS: reactive oxygen species). (B)C. neoformans and C. albicans can cross the BBB via transcytosis (I);C. neoformans can overcome the barrier paracellularly (II) or use macrophages as shuttles (macrophages as ‘Trojan horse’) (III). (C) In the lung, C. neoformans and H. capsulatum induce their own phagocytosis by innate immune cells; they can replicate intracellularly and use host cells as shuttles to reach the blood stream and subsequently escape (I and IV); evasion of C. neoformans via transcytosis (II) or crossing of C. neoformans through a compromised epithelium (III). Aspergillus spp. form hyphae, can invade endothelial cells and enter the bloodstream (V). (D)Candida spp. can escape the blood circulation after adhesion to endothelial cells (I). Candida spp. and A. fumigatus can be endocytosed (II); Candida spp. can also use fenestrated endothelium as an escape route (III) or use leukocytes as shuttles (IV). (E) In the oral cavity, C. albicans hyphae can actively penetrate the epithelium (I) and/or invade via induced endocytosis (II) or translocate paracellularly (III). (F) In the intestine, C. albicans can actively penetrate the epithelium by hyphal growth (I), translocate paracellularly (II), invade without damaging the host cell (III) or translocate via M cells by inducing endocytosis (IV). (G) In the vaginal tract, C. albicans hyphae can actively penetrate the epithelium (I) or invade via induced endocytosis (II), thereby attracting neutrophils.