CORRInsights®: Does Extracellular DNA Production Vary in Staphylococcal Biofilms Isolated From Infected Implants versus Controls?

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Excerpt

Biofilm formation is considered an important factor in determining the virulence of most implant-related infections [2]. Despite studies attempting to clarify its construction and role [4, 5], the nature of bacterial biofilms remain only partially revealed. Extracellular polymeric substances, an important part of biofilm, contribute to the organization of biofilms. However, recently, extracellular DNA (eDNA) has materialized as a possibly relevant structural component of biofilms [12]. eDNA stabilizes biofilm matrix and gene-transfer mechanisms, conditions innate immune responses, prevents phagocytosis, reduces inflammation and promotes antimicrobial resistance [5]. Although eDNA has been widely recognized as a critical factor in biofilm formation, its implications in clinical settings is less understood.
In their current study, Zatorska and colleagues found that Staphylococcus aureus and S epidermidis had differential production of eDNA with time. The difference could be due to the mechanism of eDNA release in both strains. For example, S aureus eDNA originates from cell lysis and constitutes a necessary part of biofilm development; whereas for S epidermidis, the autolysin protein AtlE mediates eDNA release and biofilm initiation.
The most-important finding of this study is that clinical isolates of S aureus and S epidermidis produced substantially more eDNA than nonclinical control isolates. Interestingly, a previous study [8] demonstrated that clinical strains of S epidermidis and the biofilm forming strain RP62A produced an abundance of eDNA compared to weak biofilm forming strains. Another study [9] examining 55 clinical isolates of S epidermidis from postsurgical and biomaterial-related orthopaedic infections showed remarkable eDNA variability. These findings indicate the presence of eDNA and its structural role in the development of biofilms in clinical strains.
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