Caspofungin-induced β(1,3)-glucan exposure in Candida albicans is driven by increased chitin levels.

ABSTRACT: To successfully induce disease, Candida albicans must effectively evade the host immune system. One mechanism used by C. albicans to achieve this is to mask immunogenic β(1,3)-glucan epitopes within its cell wall under an outer layer of mannosylated glycoproteins. Consequently, induction of β(1,3)-glucan exposure (unmasking) via genetic or chemical manipulation increases fungal recognition by host immune cells in vitro and attenuates disease during systemic infection in mice. Treatment with the echinocandin caspofungin is one of the most potent drivers of β(1,3)-glucan exposure. Several reports using murine infection models suggest a role for the immune system, and specifically host β(1,3)-glucan receptors, in mediating the efficacy of echinocandin treatment

SUBMITTER: Wagner AS 

PROVIDER: S-EPMC10470516 | biostudies-literature | 2023 Aug

REPOSITORIES: biostudies-literature