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- W4313353889 abstract "Abstract Macrophages play an important role in the quality, duration and magnitude of most inflammatory reactions in a polarized manner. However, the determinants that modulate their plasticity remain unclear. Serum amyloid A is an acute-phase protein which induces both anti-inflammatory and pro-inflammatory cytokines during inflammation. In this study, we explored the potential involvement of SAA in modulating macrophage polarization. SAA not only induced the expression of anti-inflammatory M2-specific genes such as IL-10, Arginase-1, Ym-1, Fizz-1, Mrc-1, IL-1Rn, CCL17, but also promoted efferocytosis of apoptotic neutrophils, a process that is critical for the resolution of inflammation. Through experiments with formyl peptide receptor 2 antogonist WRW4 and Fpr2 deficient macrophages, we showed that the induction of M2-specific genes and efferocytosis by SAA were mediated specifically by Fpr2. Additionally, SAA stimulation resulted in the increase expression and activation of the transcription factor interferon regulatory factor 4. Selective inhibitors of ERK activity abrogated SAA induction upon M2 macrophages and efferocytosis by decreasing the expression and activation of IRF4. Knocking down the expression of IRF4 abrogated the effect of SAA on M2 macrophage. Our results demonstrate that SAA can induce M2 macrophage-specific genes and promote efferocytosis via Fpr2-ERK-IRF4 signaling, and suggests an alternative mechanism by which SAA is involved in anti-inflammatory responses." @default.
- W4313353889 created "2023-01-06" @default.
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- W4313353889 date "2013-05-01" @default.
- W4313353889 modified "2023-09-30" @default.
- W4313353889 title "Serum amyloid A induces M2 macrophage-specific genes expression and promotes efferocytosis of apoptotic neutrophils (P5072)" @default.
- W4313353889 doi "https://doi.org/10.4049/jimmunol.190.supp.180.19" @default.
- W4313353889 hasPublicationYear "2013" @default.
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