Ex vivo and in vitro effect of serum amyloid a in the induction of macrophage M2 markers and efferocytosis of apoptotic neutrophils.
Ex vivo and in vitro effect of serum amyloid a in the induction of macrophage M2 markers and efferocytosis of apoptotic neutrophils.
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血清淀粉样蛋白 A 在诱导巨噬细胞 M2 标记物和凋亡中性粒细胞胞吞作用中的离体和体外作用
DOI：
10.4049/jimmunol.1402164
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发表时间：
2015-05-15
期刊：
影响因子：
--
通讯作者：
Ye RD
中科院分区：
文献类型：
--
作者：
Sun L;Zhou H;Zhu Z;Yan Q;Wang L;Liang Q;Ye RD
巨噬细胞以一种功能不均匀的方式影响炎症反应的大小和持续时间。巨噬细胞的表型是通过可逆的稳态机制维持的。已经确定了许多调节巨噬细胞可塑性的决定因素，尽管其确切机制尚不完全清楚。在这项研究中，我们报道了用人血清淀粉样蛋白A (SAA)（一种主要的急性期蛋白）刺激分离的人血液单核细胞和小鼠骨髓源性巨噬细胞，导致巨噬细胞M2标记物的诱导表达，包括IL-10、Ym1、Fizz-1、MRC1、IL-1Rn和CCL17。腹腔内暴露于SAA的巨噬细胞也观察到同样的效果。SAA还能提高小鼠巨噬细胞精氨酸酶1活性，增强凋亡中性粒细胞的巨噬细胞efferocysis。M2标记的诱导需要MyD88和多种信号通路的激活，但它不依赖于Stat6。SAA诱导IFN调控因子（IRF）4表达，提高其dna结合活性。用小干扰RNA沉默IRF4可消除saa诱导的M2标记物的表达。这些结果表明，SAA可能通过myd88依赖机制（涉及irf4介导的转录）改变巨噬细胞表型并调节巨噬细胞功能。
Macrophages affect the magnitude and duration of inflammatory response in a functionally heterogeneous manner. The phenotype of macrophages is maintained through a reversible homeostatic mechanism. A number of determinants that modulate macrophage plasticity have been identified, although the precise mechanisms are not fully understood. In this study, we report that stimulation of isolated human blood monocytes and mouse bone marrow–derived macrophages with human serum amyloid A (SAA), a major acute-phase protein, leads to induced expression of macrophage M2 markers, including IL-10, Ym1, Fizz-1, MRC1, IL-1Rn, and CCL17. The same effect was observed with macrophages exposed to SAA in peritoneal cavity. SAA also increases arginase 1 activity and enhances macrophage efferocytosis of apoptotic neutrophils in mouse macrophages. The induction of M2 markers requires MyD88 and the activation of multiple signaling pathways, but it is independent of Stat6. SAA induces IFN regulatory factor (IRF)4 expression and increases its DNA-binding activity. Silencing IRF4 by small interfering RNA abrogates SAA-induced expression of the M2 markers. These results suggest a potential role for SAA to alter macrophage phenotype and modulate macrophage functions through an MyD88-dependent mechanism that involves IRF4-mediated transcription.
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影响因子：
30.5
作者：
通讯作者：
--
DOI：
10.4049/jimmunol.1100500
发表时间：
2011-07-01
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Ather JL;Ckless K;Martin R;Foley KL;Suratt BT;Boyson JE;Fitzgerald KA;Flavell RA;Eisenbarth SC;Poynter ME
通讯作者：
Poynter ME
影响因子：
20.3
作者：
Gordy, Claire;Pua, Heather;He, You-Wen
通讯作者：
He, You-Wen
影响因子：
4.4
作者：
He, Rong;Shepard, Larry W.;Ye, Richard D.
通讯作者：
Ye, Richard D.
尖端：TLR2是急性阶段血清淀粉样蛋白A的功能受体。
DOI：
10.4049/jimmunol.181.1.22
发表时间：
2008-07-01
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Cheng N;He R;Tian J;Ye PP;Ye RD
通讯作者：
Ye RD