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Macrophages provide the first-line defense against invasive fungal infections and, therefore, escape from macrophage becomes the basis for the establishment of  Candida albicans  invasive infection. Here, we found that deletion of  ATP2  ( atp2 Δ/Δ) in  C. albicans  resulted in a dramatic decrease from 69.2% (WT) to 1.2% in the escape rate  in vitro . The effect of  ATP2  on macrophage clearance stands out among the genes currently known to affect clearance. In the normal mice, the  atp2 Δ/Δ cells were undetectable in major organs 72 h after systemic infection, while WT cells persisted  in vivo . However, in the macrophage-depleted mice,  atp2 Δ/Δ could persist for 72 h at an amount comparable to that at 24 h. Regarding the mechanism, WT cells sustained growth and switched to hyphal form, which was more conducive to escape from macrophages, in media that mimic the glucose-deficient environment in macrophages. In contrast,  atp2 Δ/Δ cells can remained viable but were unable to complete morphogenesis in these media, resulting in them being trapped within macrophages in the yeast form. Meanwhile,  atp2 Δ/Δ cells were killed by oxidative stress in alternative carbon sources by 2- to 3-fold more than WT cells. Taken together,  ATP2  deletion prevents  C. albicans  from escaping macrophage clearance, and therefore  ATP2  has a functional basis as a drug target that interferes with macrophage clearance.

Deletion of the ATP2 Gene in Candida albicans Blocks Its Escape From Macrophage Clearance