Fungal cytoskeleton dysfunction or immune activation triggered by beta-glucan synthase inhibitors: potential mechanisms for the prolonged antifungal activity of echinocandins.

摘要

EchinOCandinS continue to exert antifungal activity after their serum and tissue concentrations fall below what are considered therapeutic levels; possible mechanisms for this prolonged antimicrobial effect have been proposed. The echinocandin-mediated disruption of β-glucan synthesis in the fungal cell is well-regulated by Rholp, which binds guanosine triphosphate (GTP). Rholp is also a key regulatory molecule in actin synthesis, actin morphogenesis, cell wall cytoskeletal reorganization, and vesicular intracellular transport