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Review
. 2012 Feb;15(1):28-35.
doi: 10.1016/j.mib.2011.11.003. Epub 2011 Dec 1.

Host-pathogen interactions between the skin and Staphylococcus aureus

Sheila Krishna  1 , Lloyd S Miller
Affiliations
Review

Host-pathogen interactions between the skin and Staphylococcus aureus

Sheila Krishna et al. Curr Opin Microbiol. 2012 Feb.

Abstract

Staphylococcus aureus is responsible for the vast majority of bacterial skin infections in humans. The propensity for S. aureus to infect skin involves a balance between cutaneous immune defense mechanisms and virulence factors of the pathogen. The tissue architecture of the skin is different from other epithelia especially since it possesses a corneal layer, which is an important barrier that protects against the pathogenic microorganisms in the environment. The skin surface, epidermis, and dermis all contribute to host defense against S. aureus. Conversely, S. aureus utilizes various mechanisms to evade these host defenses to promote colonization and infection of the skin. This review will focus on host-pathogen interactions at the skin interface during the pathogenesis of S. aureus colonization and infection.

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Figures

Figure 1
Figure 1. Host and pathogen interactions during S. aureus colonization
A. The surface of the skin has constitutive properties such as a low temperature and pH, skin commensals and antimicrobial peptides that resist S. aureus colonization. The epidermis is composed of layers of keratinocytes, including the corneal, granular, spinous, and basal layers. There are sweat glands, sebaceous glands, and hair follicles that span these layers. In addition, there are many resident immune cells in skin that participate in immune responses, including Langerhans cells in the epidermis and dermal dendritic cells, macrophages, mast cells, T and B cells, plasma cells and NK cells in the dermis. B. S. aureus colonization requires adherence to the surface of the skin (and nasal mucosa), which is mediated by S. aureus surface components such as fibronectin-binding protein A (Fnbp A) and Fnbp B, fibrinogen-binding proteins (ClfA and ClfB), iron regulated surface determinant A (IsdA) and wall teichoic acid (WTA). Immune evasion is also mediated by IsdA, which evades host antimicrobial responses.
Figure 2
Figure 2. Pattern recognition receptors in host defense against S. aureus skin infections
A. Keratinocytes express pattern recognition receptors such as Toll-like receptor 2 (TLR2), which recognizes S. aureus lipopeptides and lipoteichoic acid, and nucleotide-binding oligomerization domain containing 2 (NOD2), which recognizes the S. aureus peptidoglycan breakdown product muramyl peptide. Both TLR2 and NOD2 signaling leads to activation of NF-κB and other transcription factors that induce transcription of proinflammatory mediators (cytokines, chemokines, adhesion molecules and antimicrobial peptides) involved in cutaneous host defense against S. aureus.
Figure 3
Figure 3. IL-1-mediated and IL17-mediated cutaneous immune response against S. aureus
S. aureus infection of skin results in production of IL-1α, IL-1β and IL-17. These proinflammatory cytokines induce keratinocyte production of antimicrobial peptides (e.g. β-defensins 2 and 3, cathelicidin, RNase 7) and cytokines, chemokines, adhesion molecules and granulopoesis factors that promote neutrophil recruitment. Recruited neutrophils from the circulation form an abscess that helps control and limit the spread of infection, which is ultimately required for bacterial clearance.
Figure 4
Figure 4. S. aureus virulence factors during cutaneous infection
S. aureus secretes several virulence factors that evade host immune defenses. α-hemolysin (or α-toxin), phenol-soluble modulins (PSMs) and Panton-Valentine leukocidin (PVL) have the capacity to lyse host cells, which is a mechanism to evade immune responses. In addition, S. aureus secretes factors that inhibit neutrophil function such as chemotaxis inhibitory protein of staphylococci (CHIPS) extracellular adherence protein (Eap). Finally, S. aureus possesses factors that inhibit reactive oxygen species (ROS)-mediated killing by neutrophils such as the golden carotenoid pigment of S. aureus and superoxide dismutase enzymes.
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