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The most common cause of infections of the skin and skin structures is Staphylococcus aureus (SSSI). The high rate of recurrent SSSI brought on by S. includes methicillin-resistant S. aureus
- Despite having high levels of specific antibodies and circulating T cells, MRSA strains of S. aureus suggest that conventional adaptive immunity only provides partial protection.
- We proposed that the protective host defense against recurrent MRSA infection involves innate immunological memory.
- SSSI was induced in wild-type and rag1-/- mice from the BALB/c and C57BL/6 backgrounds in order to test this theory.
- Reduced abscess severities and lower CFU densities compared to those in naive controls show that prior infection (priming) of wild-type and rag1-/- mice of either background provided protection against repeat infection.
- Interestingly, for wild-type and rag1-/- mice, protection was higher on the previously infected flank than on the naive flank.
- Increased infiltration of neutrophils (polymorphonuclear leukocytes [PMN]), macrophages (M), Langerin+ dendritic cells (LDC), and natural killer (NK) cells were associated with protective efficacy in wild-type mice.
- Interleukin-17A (IL-17A), IL-22, and gamma interferon (IFN-), as well as the antimicrobial peptides CRAMP and mD-3, were all related with protection.
- Additionally, priming resulted in enhanced M and LDC infiltration as well as the activation of IL-22, CRAMP, and mD-3, which protected rag1-/- mice from recurrent SSSI.
- These results imply that in recurrent MRSA SSSI, innate immunological memory, through particular cellular and molecular pathways, likely contributes to the localized host defense.
- These discoveries encourage the creation of focused immunotherapeutic approaches to deal with the problem of MRSA infection.
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