Staphylococci: Colonizers and Pathogens of Human Skin

Rosanna Coates; Josephine Moran; Malcolm J Horsburgh

Disclosures

Future Microbiol. 2014;9(1):75-91. 

In This Article

Competitive Exclusion

Several studies have identified correlated species distributions, including the absence of staphylococci from skin or nasal environments colonized by Propionibacterium acnes and Corynebacterium spp..[5,10,83] Intrageneric colonization distribution correlations were also shown in several studies for S. epidermidis and S. aureus, which were infrequently co-isolated from the nasal epithelium,[10] although this was not consistent for all studies[84] and might indicate that trait variation is important. These reports support likely exclusion mechanisms between colonizing microbiota and, for Corynebacterium spp., a proposed mechanism for S. aureus exclusion was competition for nutrients or adhesin receptors.[83] No mechanism has yet been proposed for P. acnes and S. aureus competitive exclusion; although the ability of P. acnes to exacerbate S. aureus infection[85] may indicate an immunological contribution.

The exclusion mechanisms between S. epidermidis and S. aureus have been investigated and revealed that secreted proteins of S. epidermidis, such as the serine protease Esp, stimulates keratinocyte production of hBD2 and hBD3 antimicrobials active against S. aureus, but not S. epidermidis.[84,86] Esp-secreting S. epidermidis could clear S. aureus colonization when applied intranasally. Esp disrupts S. aureus biofilms and acts synergistically with hBD2 to decrease viability of S. aureus.[84,87]

Additional exoproteins of staphylococci with antimicrobial activity targeting S. aureus and other resident and transient skin microbiota include the S. epidermidis phenol-soluble modulins (PSMs)-δ and -γ (δ-hemolysin), which are active against Group A Streptococcus, S. aureus and Escherichia coli.[88,89] Antimicrobial activity of PSM-δ and PSM-γ was synergistic with each other, with LL-37 and, in the case of PSM-γ, with CRAMP, hBD2 and hBD3.[88,89] PSM-γ is abundant on healthy human skin and reduced bacterial load in a mouse Group A Streptococcus skin wound infection model, indicating physiological relevance.[88]S. aureus PSMs possess limited antimicrobial activity; instead, their role is linked to biofilm structuring, hemolysis, spreading over wet surfaces and possibly promoting skin colonization.[90,91] It remains to be determined whether other staphylococcal PSMs resemble S. epidermidis or S. aureus in their potential to promote colonization through antagonism.

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