4. Staphylococcus
S. Afermentans
S. aureus
S. auricularis
S. capitis
S. caprae
S. carnosus
S. cohnii
S. epidermidis
S. Felis
S. haemolyticus
S. hominis
S. intermedius
S. lugdunensis
S. pettenkoferi
S. saprophyticus
S. schleiferi
S. sciuri
S. simulans
S. vitulus
S. warneri
S. xylosus
11. | Epidermal keratinocytes constitutively contain stores of pre-made interleukin-1α (IL-
1α) during resting conditions, which is rapidly released in response to nonspecific
injury, inflammation or infection. b | In keratinocytes, Staphylococcus aureus induces
an IL-1α-mediated autocrine signalling loop through IL-1 receptor 1 (IL-1R1), which
leads to the rapid and continuous production of neutrophil-attracting chemokines,
such as CXC-chemokine ligand 1 (CXCL1), CXCL2 and CXCL8. c | The production of IL-1β
during S. aureus cutaneous infections requires two signals. Signal 1 involves the
transcription of pro-IL-1β, which is induced by the activation of pattern recognition
receptors (PRRs), such as TLR2 (Toll-like receptor 2) and NOD2 (nucleotide-binding
oligomerization domain-containing protein 2). Signal 2 involves NLRP3 (NOD-, LRR- and
pyrin domain-containing 3) inflammasome activation, which results in caspase 1-
mediated cleavage of pro-IL-1β into active IL-1β. NLRP3 inflammasome activation
during S. aureus infections has been shown to be triggered by lysozyme-mediated
digestion of S. aureus (which releases peptidoglycan, induces the production of
reactive oxygen intermediates and promotes phagosome rupture), by the activation of
the purinergic receptor P2X7 by ATP (which is released by stressed or damaged cells
during an infection) and by pore-forming toxins of S. aureus, such as the α-, β- and γ-
haemolysins. IκB, inhibitor of NF-κB; MDP, muramyl dipeptide; NF-κB, nuclear factor-
κB.
