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Resident macrophages acquire innate immune memory in staphylococcal skin infection.


ABSTRACT: Staphylococcus aureus (S. aureus) is a common colonizer of healthy skin and mucous membranes. At the same time, S. aureus is the most frequent cause of skin and soft tissue infections. Dermal macrophages (M?) are critical for the coordinated defense against invading S. aureus, yet they have a limited life span with replacement by bone marrow derived monocytes. It is currently poorly understood whether localized S. aureus skin infections persistently alter the resident M? subset composition and resistance to a subsequent infection. In a strictly dermal infection model we found that mice, which were previously infected with S. aureus, showed faster monocyte recruitment, increased bacterial killing and improved healing upon a secondary infection. However, skin infection decreased M? half-life, thereby limiting the duration of memory. In summary, resident dermal M? are programmed locally, independently of bone marrow-derived monocytes during staphylococcal skin infection leading to transiently increased resistance against a second infection.

SUBMITTER: Feuerstein R 

PROVIDER: S-EPMC7343389 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature

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<i>Staphylococcus aureus (S. aureus)</i> is a common colonizer of healthy skin and mucous membranes. At the same time, <i>S. aureus</i> is the most frequent cause of skin and soft tissue infections. Dermal macrophages (Mφ) are critical for the coordinated defense against invading <i>S. aureus,</i> yet they have a limited life span with replacement by bone marrow derived monocytes. It is currently poorly understood whether localized <i>S. aureus</i> skin infections persistently alter the resident  ...[more]

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