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The role of proteinaceous toxins secreted by Staphylococcus aureus in interbacterial competition

Lookup NU author(s): Stephen Garrett, Professor Tracy Palmer FRS FRSE FMedSciORCiD

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This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).


Abstract

© 2024 The Author(s). Published by Oxford University Press on behalf of FEMS. Staphylococcus aureus is highly adapted to colonization of the mammalian host. In humans the primary site of colonization is the epithelium of the nasal cavity. A major barrier to colonization is the resident microbiota, which have mechanisms to exclude S. aureus. As such, S. aureus has evolved mechanisms to compete with other bacteria, one of which is through secretion of proteinaceous toxins. S. aureus strains collectively produce a number of well-characterized Class I, II, and IV bacteriocins as well as several bacteriocin-like substances, about which less is known. These bacteriocins have potent antibacterial activity against several Gram-positive organisms, with some also active against Gram-negative species. S. aureus bacteriocins characterized to date are sporadically produced, and often encoded on plasmids. More recently the type VII secretion system (T7SS) of S. aureus has also been shown to play a role in interbacterial competition. The T7SS is encoded by all S. aureus isolates and so may represent a more widespread mechanism of competition used by this species. T7SS antagonism is mediated by the secretion of large protein toxins, three of which have been characterized to date: A nuclease toxin, EsaD; a membrane depolarizing toxin, TspA; and a phospholipase toxin, TslA. Further study is required to decipher the role that these different types of secreted toxins play in interbacterial competition and colonization of the host.


Publication metadata

Author(s): Garrett SR, Palmer T

Publication type: Review

Publication status: Published

Journal: FEMS Microbes

Year: 2024

Volume: 5

Online publication date: 28/02/2024

Acceptance date: 27/02/2024

ISSN (electronic): 2633-6685

Publisher: Oxford University Press

URL: https://doi.org/10.1093/femsmc/xtae006

DOI: 10.1093/femsmc/xtae006


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