MyD88 in macrophages is critical for abscess resolution in staphylococcal skin infection
13.02.2015
Feuerstein R, Seidl M, Prinz M, Henneke P.
J Immunol. 2015 Mar 15;194(6):2735-45
When Staphylococcus aureus penetrates the epidermis and reaches the dermis, polymorphonuclear leukocytes (PMLs) accumulate and an abscess is formed. However, the molecular mechanisms that orchestrate initiation and termination of inflammation in skin infection are incompletely understood. In this study, we found that MyD88-dependent sensing of S. aureus by dermal macrophages (M?) contributes to both timely escalation and termination of PML-mediated inflammation in a mouse model of staphylococcal skin infection. Taken together, MyD88-dependent sensing of staphylococci by resident dermal M?s is key for a rapid and balanced immune response, and PMLs are dependent on intact M? for full function. Renewal of resident M?s requires both local control of bacteria and inflammatory monocytes entering the skin.
