Dynamic interactions between dermal macrophages and Staphylococcus aureus

Abstract

The dermis, a major reservoir of immune cells in immediate vicinity to the colonizing skin microflora, serves as an important site of host-pathogen interactions. Macrophages (Mϕ) are the most frequent resident immune cell type in the dermis. They protect the host from invasive infections by highly adapted bacteria, such as staphylococci via pattern recognition of bacterial effectors, phagocytosis, and recruitment of other myeloid cells from the blood. Already under homeostatic conditions, the dermal Mϕ population receives a dynamic input of monocytes invading from the bloodstream. This quantitative renewal is promoted further at the beginning of life, when prenatally seeded cells are rapidly replaced and in healing phases after injuries or infections. Here, we discuss the potential implications of the dynamic dermal Mϕ biology on the establishment and maintenance of immunity against Staphylococcus aureus, which can either be a harmless colonizer or an invasive pathogen. The understanding of the heterogeneity of the "mature" dermal Mϕ compartment driven both by the influx of differentiating monocytes and by a bone marrow-independent Mϕ persistence and expansion may help to explain failing immunity and immunopathology originating from the skin, the important interface between host and environment.

Detecting Chronic Post-Traumatic Osteomyelitis of Mouse Tibia via an IL-13Rα2 Targeted Metallofullerene Magnetic Resonance Imaging Probe

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Targeting mononuclear phagocytes for eradicating intracellular parasites

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Skin Immune Landscape: Inside and Outside the Organism

“…The host's defense against S. aureus includes (i) the skin barrier and outcompetition with other strains, for example, S. epidermidis , as described previously; (ii) the innate immune responses, mostly driven by antimicrobial peptide (AMP), complement, neutrophil, and macrophage activation; and (iii) the adaptive immune response. S. aureus is an excellent model of bacteria being part of a semiresident flora, but able to switch as a pathogen as soon as it is left uncontrolled by other members of resident flora [ 33 – 36 ]. The coevolution of this particular microorganism with the host's SIS and its ability to get specific virulence genes easily and rapidly makes it a quite interesting target to understand how this system is dynamic.…”