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

Adhesins Facilitate Niche Selection

The breadth of adhesins and their differential specificity accounts for host and tissue specificity (Table 1). The S. epidermidis RP62A genome encodes 12 MSCRAMMS, whereas S. aureus can express up to 20.[29] This varied repertoire could explain colonization differences between the otherwise similar S. aureus and S. epidermidis.[30] For example, the homologous MSCRAMMs Aap of S. epidermidis and SasG of S. aureus mediate adhesion to different niches. While Aap can bind buccal epithelial cells and desquamated corneocytes, SasG binds desquamated nasal cells, but not buccal epithelial or keratinocyte cells.[31,32] It is likely that the receptor is the same, since recombinant Aap could block SasG adhesion;[31] however, Aap must be more promiscuous in its binding. This difference could indicate that Aap is adapted for colonization of skin and nares; however, it could also be an artifact caused by different methodologies and cell origin.

A study of adhesion to layers of the stratum corneum by S. epidermidis identified three patterns of binding. First binding to superficial, fully differentiated corneocytes and hairs; second, binding to deeper, less differentiated epithelia at cell–cell junctions; and finally universal binding to all layers across the entire surface of the cell.[33] Binding to different layers of the stratum corneum owing to receptor variation between skin layers could affect long-term colonization or survival.

Variation between cell layer receptors is an important consideration since most studies examine adhesion to desquamated corneocytes or less differentiated keratinocyte cell lines, but not both together. Human skin components known to act as staphylococcal adhesin receptors are listed in Table 1. Of these receptors, loricrin is a major component of the cornified envelope, and as such, is present on the periphery of corneocytes in the stratum corneum (Figure 1). Another of these receptors, involucrin, is expressed at the cell periphery in the stratum spinosum, stratum granulosum and stratum corneum.[34] Differences in receptor expression between layers of the skin highlights the importance of choice of cell type in bacterial adhesion assays.

Intraspecies variation between adhesins explains staphylococcal host and target cell range. In a study of 28 S. epidermidis isolates of human origin, there was no significant adhesion to bovine udder stratum corneum, whereas the majority (26/28) adhered to human stratum corneum.[33] Staphylococci of canine, feline or bovine origin were shown to adhere to a similar extent to human and canine skin, but differed significantly in adhesion to feline skin.[35] Skin diseases affect colonization. Most notably, S. aureus and S. intermedius exhibit increased binding to atopic human and canine skin, respectively.[36,37] In humans, enhanced binding was primarily due to the enhanced levels of fibronectin present in atopic skin, compared with healthy or psoriatic skin, and was mediated by the S. aureus MSCRAMMs FnbpA, FnbpB, ClfA and ClfB.[37]

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