Abstract
The incidence of invasive fungal infections is increasing worldwide, resulting in more than 1.6 million deaths every year. Due to growing antifungal drug resistance and the limited number of currently used antimycotics, there is a clear need for novel antifungal strategies. In this context, great potential is attributed to antimicrobial peptides (AMPs) that are part of the innate immune system of organisms. These peptides are known for their broad-spectrum activity that can be directed toward bacteria, fungi, viruses, and/or even cancer cells. Some AMPs act via rapid physical disruption of microbial cell membranes at high concentrations causing cell leakage and cell death. However, more complex mechanisms are also observed, such as interaction with specific lipids, production of reactive oxygen species, programmed cell death, and autophagy. This review summarizes the structure and mode of action of antifungal AMPs, thereby focusing on their interaction with fungal membranes.
Highlights
In the past two decades, fungal infections have caused severe die-offs and extinctions in wild species, as they comprise the biggest threat for both plant (64%) and animal (72%) species in terms of infection-related species extinctions (Fisher et al, 2012)
antimicrobial peptides (AMPs) is demonstrated in vivo as exemplified by RsAFP2’s activity in a prophylactic murine model of candidiasis and by the histatin 5 derivative P113’s activity against oral candidiasis that completed clinical phase IIb (Tavares et al, 2008; Brunetti et al, 2016; Håkansson et al, 2019; Mookherjee et al, 2020)
Inactivation of AMPs by cations upon systemic administration could be limiting for commercial applications, alternative administration routes, such as topical administration, in which the inactivation of AMPs by cations is of less importance, could be of interest
Summary
In the past two decades, fungal infections have caused severe die-offs and extinctions in wild species, as they comprise the biggest threat for both plant (64%) and animal (72%) species in terms of infection-related species extinctions (Fisher et al, 2012).
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