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Staphylococcus epidermidisis predominant in implant-associated infections due to its capability to form biofilms. It can deploy several strategies for biofilm development using either polysaccharide intercellular adhesin (PIA), extracellular DNA (eDNA) and/or proteins, such as the extracellular matrix-binding protein (Embp).    Hypothesis/Gap Statement  We hypothesize that the dichotomic regulation ofS. epidermidisadhesins is linked to whether it is inside a host or not, and that  in vitro  biofilm investigations in laboratory media may not reflect actual biofilms  in vivo .    Aim   We address the importance of PIA and Embp in biofilm grown in ‘humanized’ media to understand if these components play different roles in biofilm formation under conditions where bacteria can incorporate host proteins in the biofilm matrix.    MethodologyS. epidermidis1585 WT (deficient in  icaADBC ), and derivative strains that either lack  embp , express  embp  from an inducible promotor, or express  icaADBC  from a plasmid, were cultivated in standard laboratory media, or in media with human plasma or serum. The amount, structure, elasticity and antimicrobial penetration of biofilms was quantified to describe structural differences caused by the different matrix components and growth conditions. Finally, we quantified the initiation of biofilms as suspended aggregates in response to host factors to determine how quickly the cells aggregate in response to the host environment and reach a size that protects them from phagocytosis.    ResultsS. epidermidis1585 required polysaccharides to form biofilm in laboratory media. However, these observations were not representative of the biofilm phenotype in the presence of human plasma. If human plasma were present, polysaccharides and Embp were redundant for biofilm formation. Biofilms formed in human plasma were loosely attached and existed mostly as suspended aggregates. Aggregation occurred after 2 h of exposing cells to plasma or serum. Despite stark differences in the amount and composition of biofilms formed by polysaccharide-producing and Embp-producing strains in different media, there were no differences in vancomycin penetration or susceptibility.    Conclusion.   We suggest that the assumed importance of polysaccharides for biofilm formation is an artefact from studying biofilms in laboratory media void of human matrix components. The cell–cell aggregation ofS. epidermidiscan be activated by host factors without relying on either of the major adhesins, PIA and Embp, indicating a need to revisit the basic question of howS. epidermidisdeploys self-produced and host-derived matrix components to form antibiotic-tolerant biofilms  in vivo .

Host factors abolish the need for polysaccharides and extracellular matrix-binding protein in Staphylococcus epidermidis biofilm formation