Resident macrophages acquire innate immune memory in staphylococcal skin infection

Area of Science:

• Immunology
• Dermatology
• Microbiology

Background:

• Staphylococcus aureus (S. aureus) is a common skin colonizer and a frequent cause of skin infections.
• Dermal macrophages (Mφ) are crucial for combating S. aureus but have a limited lifespan, being replaced by monocytes.
• The long-term effects of S. aureus skin infections on resident Mφ populations and subsequent infection resistance are not well understood.

Purpose of the Study:

• To investigate whether localized S. aureus skin infections alter resident dermal macrophage (Mφ) subsets and influence resistance to secondary infections.
• To determine if dermal Mφ are programmed locally during S. aureus infection, independent of bone marrow-derived monocytes.

Main Methods:

• Utilized a murine model of strictly dermal Staphylococcus aureus infection.
• Assessed monocyte recruitment, bacterial killing, wound healing, and Mφ half-life following primary and secondary infections.

Main Results:

• Mice with prior S. aureus infection exhibited faster monocyte recruitment, enhanced bacterial killing, and improved healing during secondary infections.
• Primary S. aureus skin infection reduced the half-life of dermal macrophages (Mφ), indicating a transient protective memory.
• These effects were mediated by locally programmed dermal Mφ, independent of bone marrow-derived monocytes.

Conclusions:

• Localized Staphylococcus aureus skin infection induces a transiently enhanced resistance to secondary infections.
• Resident dermal macrophages (Mφ) are locally programmed during infection, contributing to improved defense mechanisms.
• The protective effect is limited by a decreased Mφ half-life, suggesting a finite duration of this enhanced resistance.