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- W4366185370 abstract "Staphylococcus aureus is the leading cause of skin and soft tissue infections. With the emergence of antibiotic-resistant bacteria, there is an unmet clinical need to develop novel therapies to treat skin infections. The inflammasome components involved in response to S. aureus stimulation are well established in in vitro immune cell cultures. However, the inflammasome formation in immune cells during in vivo S. aureus skin infections are not entirely understood. Therefore, we used an in vivo mouse model of S. aureus intradermal infection to first define the immune cells with inflammasome formation during S. aureus skin infections. Using an ASC-Citrine reporter mouse, we observed neutrophils as the predominant inflammasome-forming population in the infected skin. To elucidate the inflammasome-associated nod-like receptor, we used NLRP3, AIM2, or NLRC4-deficient mice, but unexpectedly found no host defense defect compared to WT mice. However, by performing co-immunoprecipitations from infected skin biopsies, we discovered that the inflammasome sensor, NLRP12, associated with the ASC adaptor protein. Next, we set out to identify the inflammasome-associated caspases by infecting caspase-1, -11, and caspase-1/11 double-deficient mice but observed no significant difference in host defense compared to WT mice. Thus, we generated S100A8Cre-Casp8fl/fl mice (neutrophil-specific deletion of caspase-8) and discovered a significant host defense defect compared to WT mice. Collectively, our data indicated that NLRP12 and caspase-8 inflammasome signaling in neutrophils was critical for protection against S. aureus skin infections, providing potential therapeutic targets." @default.
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- W4366185370 date "2023-05-01" @default.
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- W4366185370 title "1050 Neutrophil-intrinsic NLRP12 and caspase-8 signal for inflammasome-mediated host defense against staphylococcus aureus skin infections" @default.
- W4366185370 doi "https://doi.org/10.1016/j.jid.2023.03.1061" @default.
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