CD16+ monocytes produce IL-6, CCL2, and matrix metalloproteinase-9 upon interaction with CX3CL1-expressing endothelial cells
CD16+ monocytes produce IL-6, CCL2, and matrix metalloproteinase-9 upon interaction with CX3CL1-expressing endothelial cells
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DOI：
10.1189/jlb.0206125
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发表时间：
2006-11-01
影响因子：
5.5
通讯作者：
Gabuzda, Dana
中科院分区：
文献类型：
--
作者：
Ancuta, Petronela;Wang, Jianbin;Gabuzda, Dana
在包括败血症、HIV-1感染和癌症在内的炎症条件下，外周血单核细胞（Mo）的CD16（+）亚群急剧扩增。CD16（+）表达高水平的CX3CR1，在流动条件下介导表达CX3CR1的内皮细胞（EC）的阻滞。相比之下，CD16(-) Mo附着在细胞因子激活的EC上不依赖于CX3CL1。在这里，我们研究了CD16（+）和CD16(-) Mo与表达cx3cl1的HUVEC相互作用时产生促炎细胞因子的能力。我们证明CD16（+）而不是CD16(-) Mo在与TNF/ ifn - γ激活的HUVEC或表达CX3CL1的非激活的HUVEC共培养时产生高水平的IL-6、CCL2和基质金属蛋白酶(MMP)-9。此外，Mo上清液与细胞因子激活的HUVEC共培养可诱导体外神经元死亡。这些结果表明，膜结合的CX3CL1刺激CD16(+) Mo产生IL-6、CCL2和MMP-9，可能是通过CX3CR1的参与。因此，CD16(+) Mo的扩增及其在表达cx3cl1的EC上的积累可能导致Mo和T细胞亚群在炎症部位募集，以响应CCL2、il -6诱导的细胞活化和/或分化，以及mmp -9介导的血管和组织损伤。j . Leukoc。生物学杂志。80:1156-1164；2006.
The CD16(+) subset of peripheral blood monocytes (Mo) is expanded dramatically during inflammatory conditions including sepsis, HIV-1 infection, and cancer. CD16(+) express high levels of CX3CR1, which mediates arrest onto CX3CL1-expressing endothelial cells (EC) under flow conditions. In contrast, attachment of CD16(-) Mo onto cytokine-activated EC is independent of CX3CL1. Here, we investigate the ability of CD16(+) and CD16(-) Mo to produce proinflammatory cytokines upon interaction with CX3CL1-expressing HUVEC. We demonstrate that CD16(+) but not CD16(-) Mo produce high levels of IL-6, CCL2, and matrix metalloproteinase (MMP)-9 when cocultured with TNF/IFN-gamma-activated HUVEC or nonactivated HUVEC expressing CX3CL1. Furthermore, supernatants from Mo cocultured with cytokine-activated HUVEC induce neuronal death in vitro. These results suggest that membrane-bound CX3CL1 stimulates production of IL-6, CCL2, and MMP-9 by CD16(+) Mo, likely via engagement of CX3CR1. Thus, expansion of CD16(+) Mo and their accumulation onto CX3CL1-expressing EC may result in recruitment of Mo and T cell subsets at sites of inflammation in response to CCL2, IL-6-induced cell activation and/or differentiation, and MMP-9-mediated vascular and tissue injury. J. Leukoc. Biol. 80: 1156-1164; 2006.