The role of macrophages in S. aureus colonization of inflammatory skin diseases

01.03.2025 bis 29.02.2028

Atopic dermatitis (AD) and psoriasis (Ps) are inflammatory skin diseases that affect 3-10% of individuals worldwide. Ps and AD are both triggered by a specific pathological T cell immune response. Tissue-resident macrophages are important for tissue homeostasis and tissue remodeling and are key players in the inflammatory immune response of the skin and in the primary defense against pathogens. They play essential roles in antigen presentation, phagocytosis, and immunomodulation through production of cytokines and growth factors. When exposed to microenvironmental stimuli, macrophages can polarize into the pro-inflammatory M1-type and the anti-inflammatory M2-type, both of which perform largely opposing functions. Lesional skin of AD patients are often colonized by S. aureus, whereas psoriatic skin is only rarely colonized by S. aureus. Staphylococcal skin infections are one of the most common complications in AD and further drive the disease. Professional phagocytes, primarily macrophages and neutrophils, are key innate immune cells which interact with S. aureus, acting as gatekeepers to resolve the infection. Recent studies have highlighted the important roles of macrophages during S. aureus infections using a wide array of killing mechanisms. In defense, S. aureus has evolved multiple strategies to survive within, manipulate and escape from macrophages, allowing them to not only subvert but also exploit them. Macrophage - S. aureus interactions are multifaceted and have direct roles in infection outcome. In depth understanding of these host-pathogen interactions is therefore required to develop novel therapeutic strategies.