Figure 1: Interactions between Staphylococcus aureus,
native skin commensals and host cells in healthy or diseased skin.
On healthy skin (left), commensals like coagulase-negativeStaphylococcus (CoNS) and the fungi Malassezia secrete a
variety of compounds to inhibit the growth of the pathobiontStaphylococcus aureus (S. aureus ). CoNS secrete phenol
soluble modulins (PSMs) and auto-inducing peptides, which inhibitS. aureus growth and virulence factor expression respectively.
CoNS can stimulate host epidermal cells to produce anti-microbial
peptides (AMPs) to further restrain S. aureus growth. Both CoNS
and commensal Malassezia also secrete a variety of proteases,
which disrupt S. aureus biofilm formation. These mechanisms
contribute to T cell tolerance and likely optimize barrier function on
healthy skin. On inflamed skin (right), increased S. aureuscolonization and biofilm formation can lead to heightened secretion of
virulence factors such as PSMs, toxins and proteases that damage the
stratum corneum. Host AMPs are present in lower amounts or are rendered
less effective due to S. aureus activity and Th2 signalling.S. aureus can also suppress the growth or activity of skin
commensals. Superantigens released by S. aureus can penetrate the
epidermis and trigger dermal dendritic cells to drive T helper 2 (Th2)
polarization and expansion. Excessive numbers of Th2 cells in turn,
produce a variety of pro-inflammatory cytokines, which further
exacerbate skin barrier dysfunction, IgE production by B-cells and mast
cell degranulation. While the pre-flare skin (middle) is not inflamed,
there might be decreases in the abundance of commensals which inhibitS. aureus , promoting its transition to a pathogenic state. These
individuals have elevated Th2 responses and IgE compared to healthy
skin, and are pre-disposed to severe itching in subsequent flares.
(Created with BioRender.com)