Structural basis of Staphylococcus epidermidis biofilm formation: mechanisms and molecular interactions

Abstract

Staphylococcus epidermidis is a usually harmless commensal bacterium highly abundant on the human skin. Under defined predisposing conditions, most importantly implantation of a medical device, S. epidermidis, however, can switch from a colonizing to an invasive life style. The emergence of S. epidermidis as an opportunistic pathogen is closely linked to the biofilm forming capability of the species. During the past decades, tremendous advance regarding our understanding of molecular mechanisms contributing to surface colonization has been made, and detailed information is available for several factors active during the primary attachment, accumulative or dispersal phase of biofilm formation. A picture evolved in which distinct factors, though appearing to be redundantly organized, take over specific and exclusive functions during biofilm development. In this review, these mechanisms are described in molecular detail, with a highlight on recent insights into multi-functional S. epidermidis cell surface proteins contributing to surface adherence and intercellular adhesion. The integration of distinct biofilm-promoting factors into regulatory networks is summarized, with an emphasis on mechanism that could allow S. epidermidis to flexibly adapt to changing environmental conditions present during colonizing or invasive life-styles.

Staphylococcus epidermidis small basic protein (Sbp) forms amyloid fibrils, consistent with its function as a scaffolding protein in biofilms

“…In contrast with its more virulent cousin Staphylococcus aureus, which produces an abundance of toxins, adherence factors, and cytolysins, the main virulence mechanism through which Staphylococcus epidermidis evade the host immune response relates to its capability of adhering and forming biofilms on biotic and abiotic surfaces (3). Staphylococcal biofilms are adherent multilayered communities of multicellular organisms embedded in self-produced extracellular matrix that are functionally resistant to antibiotics and components of the immune system (4).…”

“…Although the polycationic polysaccharide intercellular adhesion (PIA), which is synthesized by the icaADBC operon that widely distributes in clinical S. epidermidis isolates, have long been identified as a major component of the biofilm matrix and considered as the major intercellular adhesin in staphylococci biofilm formation, not all strains of S. epidermidis carry the icaADBC operon, it is now clear that protein-based matrices also have the ability to mediate biofilm accumulation and cause infection in an ica-independent manner (6,8). In S. epidermidis, one well studied among these biofilm matrix proteins is accumulation-associated protein (Aap), which is a cell wall-anchored, multi-domain, multifunctional surface protein with significant roles in biofilm formation (3,4,9). Aap consists of an N-terminal Domain-A with a variable number of 16-aa repeats located N terminally and a putative L-type lectin subdomain, a C-terminal Domain-B composed of between 3 and 17 nearly identical 128-aa B repeats terminating in a conserved "half repeat" motif.…”

Determinación de factores de adhesión asociados a la formación de biopelícula en aislamientos clínicos de Staphylococcus aureus y Staphylococcus epidermidis

“…Se sugiere que las cepas de relevancia clínica contienen plásmidos conjugativos que facilitan la formación de la biopelícula; un ejemplo de ello es Escherichia coli, que codifica el plásmido F que actúa como un factor de adhesión en la superficie celular actuando en las interacciones de célula a célula para la conformación de biopelículas (34). No obstante es importante mencionar que muchos organismos que no pueden transportar plás-midos producen solo microcolonias pero no biopelícula, pero cuando estos organismos reciben plásmidos de bacterias donantes, estos empiezan a producir biopelículas (35)(36)(37).…”

Efficcacy of Lantana camara Linn. leaf extracts ointment on dermal wound healing were infected with Staphylococcus epidermidis

“…This opinion is consistent with the statement that S. epidermidis as an opportunistic pathogen is closely linked to the biofilm forming capability of the species. 31 Further explained that in the process of biofilm formation, there is increased activity of bacteria to break down the extracellular matrix host. 32 The event is important that in chronic wounds has been the prolongation of the inflammatory phase of repair.…”