Figure 2.

sCD163 modulates the host defense against staphylococcal infections. During sepsis membrane bound CD163 undergoes ectodomain shedding that leads to the generation of the soluble form of CD163 (sCD163). This process is mediated via cleavage by metalloproteinase TACE/ADAM17. S. aureus adheres to host tissue by binding of fibronectin. Once released, sCD163 also recognizes and binds to fibronectin, which then acts as a bridge between sCD163 and the staphylococci. This binding promotes the effective clearance (enhanced phagocytosis and killing) of S. aureus by professional phagocytes, while dampening the induction of proinflammatory cytokines and subsequently protecting the host from overwhelming inflammation.