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However, macrophages are unable to kill fungal spores (Levitz et al., 1986; Waldorf, 1989).
In the experimental setting, LC T/MCT and MCTincrease monocyte adhesion and degranulation [ 31, 32], whereas another study reported decreased neutrophil capacity to kill fungal pathogens [ 33].
This was the case following exposure to macrophages, which play an important defensive role during infections of parenchyma, and to neutrophils, which kill fungal cells present in the bloodstream.
Because the 39-kDa and the 40-kDa chitotriosidases do not have a chitin-binding domain, they cannot react to the native form of chitin and, therefore, cannot kill fungal cells [16], [17].
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It is shown that VG16KRKP kills fungal cells mainly through membrane compromise leading to efflux of ions and cell metabolites.
For instance, it kills fungal cells through the induction of cAMP and bacterial cells by damaging the membrane [ 14, 18].
Despite its efficacy in killing fungal cells, the use of AmB for treating fungal infections in the central nervous system (CNS) has proven challenging.
Our data are consistent with the idea that genes involved in central carbon metabolism are more active in C. albicans cells engulfed by neutrophils, although neutrophils are thought to be more potent than macrophages at killing fungal cells (Fradin et al., 2005).
Nystatin binds to ergosterol before it punches holes in the membrane and selectively kills fungal cells.
A concentrations of 4-6% of hypochlorite, found in household bleach, not only inhibits the growth of molds, but also kills fungal colonies of Aspergillus niger.
Our results reveal catheters coated with β-peptide-loaded multilayers to kill planktonic fungal cells for up to 21 days of intermittent challenges with C. albicans and prevent biofilm formation on catheter walls for at least 48 h.
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