Background

Staphylococcus epidermidis has long been known as a major bacterial coloniser of the human skin, yet it is also a prominent nosocomial pathogen. Its remarkable ability to assemble structured biofilms has been its major known pathogenic feature to date. Notwithstanding important discoveries that have been accomplished, several questions about S. epidermidis biofilm formation still remain to be elucidated. This study aimed to assess whether iron availability modulates S. epidermidis biofilm formation and, if so, to explore how such modulation occurs. Biofilms of three S. epidermidis strains were grown under iron-enriched/-deficient conditions and several physiologic and transcriptomic changes were assessed. Our data revealed that while physiologic iron levels do not compromise biofilm formation, iron excess or deficiency is detrimental for this process. Conversely, biofilm cells were not affected in the same way when grown planktonically. By studying biofilm cells in detail we found that their viability and cultivability were seriously compromised by iron deficiency. Also, a temporal analysis of biofilm formation revealed that iron excess/deficiency: i) impaired biomass accumulation from 6h onwards, and ii) induced changes in the biofilm structure, indicating that iron availability plays a pivotal role from an early biofilm development stage. The expression of several putative iron-related genes, namely encoding siderophore biosynthesis/transport-related proteins, was found to be modulated by iron availability, providing a biological validation of their function on S. epidermidis iron metabolism. This study therefore provides evidence that iron plays a pivotal role on S. epidermidis biofilm formation.

These results reinforce the concept that S. epidermidis is an 'accidental pathogen,' and that the ica operon is the main mechanism of biofilm formation in clinical and commensal isolates.

Coagulase-negative staphylococci (CoNS) are common bacterial colonizers of the human skin. They are often involved in nosocomial infections due to biofilm formation in indwelling medical devices. While biofilm formation has been extensively studied in Staphylococcus epidermidis, little is known regarding other CoNS species. Here, biofilms from six different CoNS species were characterized in terms of biofilm composition and architecture. Interestingly, the ability to form a thick biofilm was not associated with any particular species, and high variability on biofilm accumulation was found within the same species. Cell viability assays also revealed different proportions of live and dead cells within biofilms formed by different species, although this parameter was particularly similar at the intraspecies level. On the other hand, biofilm disruption assays demonstrated important inter- and intraspecies differences regarding extracellular matrix composition. Lastly, confocal laser scanning microscopy experiments confirmed this variability, highlighting important differences and common features of CoNS biofilms. We hypothesized that the biofilm formation heterogeneity observed was rather associated with biofilm matrix composition than with cells themselves. Additionally, our results indicate that polysaccharides, DNA and proteins are fundamental pieces in the process of CoNS biofilm formation.