Abstract

Staphylococcus aureus is an opportunistic pathogen that colonizes the skin and mucosal surfaces of mammals. Persistent staphylococcal infections often involve surface-associated communities called biofilms. Here we report the discovery of a novel extracellular fibril structure that promotes S. aureus biofilm integrity. Biochemical and genetic analysis has revealed that these fibers have amyloid-like properties and consist of small peptides called phenol soluble modulins (PSMs). Mutants unable to produce PSMs were susceptible to biofilm disassembly by matrix degrading enzymes and mechanical stress. Previous work has associated PSMs with biofilm disassembly, and we present data showing that soluble PSM peptides disperse biofilms while polymerized peptides do not. This work suggests the PSMs' aggregation into amyloid fibers modulates their biological activity and role in biofilms.

Highlights

  • Staphylococcus aureus is the causative agent of numerous diseases ranging from relatively benign skin conditions to fatal systemic infections

  • We demonstrate that S. aureus produces extracellular fibers in multicellular biofilm communities, and that these fibers help the bacterial community to withstand physical stresses

  • These fibers consist of small peptides called phenol soluble modulins (PSMs) that have previously been implicated in biofilm disassembly and virulence

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Summary

Introduction

Staphylococcus aureus is the causative agent of numerous diseases ranging from relatively benign skin conditions to fatal systemic infections. Formation of bacterial biofilms on host tissues and implanted materials contributes to chronic S. aureus infections, as biofilms are exceptionally resistant to host immune response and chemotherapies [1]. We examined how growth media affects the composition of the biofilm matrix. This led to the discovery of an extracellular fibril structure in S. aureus biofilms grown in a nonstandard rich media. These fibers share morphological and biophysical characteristics with functional bacterial amyloids such as curli in Escherichia coli biofilms, TasA of Bacillus subtilis, and the Fap fimbriae in Pseudomonas aeruginosa [13,14,15,16]. Mutants incapable of producing PSMs formed biofilms that were susceptible to disassembly by enzymatic degradation and mechanical stress

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