Protective actions of aspirin-triggered (17R) resolvin D1 and its analogue, 17R-hydroxy-19-para-fluorophenoxy-resolvin D1 methyl ester, in C5a-dependent IgG immune complex-induced inflammation and lung injury.
Protective actions of aspirin-triggered (17R) resolvin D1 and its analogue, 17R-hydroxy-19-para-fluorophenoxy-resolvin D1 methyl ester, in C5a-dependent IgG immune complex-induced inflammation and lung injury.
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DOI：
10.4049/jimmunol.1400942
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发表时间：
2014-10-01
期刊：
影响因子：
--
通讯作者：
Gao H
中科院分区：
文献类型：
--
作者：
Tang H;Liu Y;Yan C;Petasis NA;Serhan CN;Gao H
越来越多的证据表明，新型抗炎和促消退介质如消退素在炎症过程中起重要作用。然而，这些脂质介质在免疫复合物（IC）诱导的肺损伤中的功能仍不清楚。在这里，我们确定了阿司匹林触发的消退素D1（AT-RvD 1）及其代谢稳定的类似物，17 R-羟基-19-对氟苯氧基-消退素D1甲酯（p-RvD 1），在IgG IC诱导的骨髓细胞炎症反应和肺损伤中的作用。我们发现，在AT-RvD 1或p-RvD 1治疗的小鼠的肺血管通透性显着降低时，在损伤期间接受对照囊泡的小鼠相比。此外，静脉注射AT-RvD 1或p-RvD 1可显著降低支气管肺泡灌洗液（BALF）中中性粒细胞、炎性细胞因子和趋化因子的含量。有趣的是，AT-RvD 1或p-RvD 1显著降低BALF补体C5 a水平。通过电泳迁移率改变实验，我们证明AT-RvD 1和p-RvD 1能显著抑制IgG IC诱导的肺组织NF-κB和C/EBPβ转录因子的激活。此外，AT-RvD 1显著减轻IgG IC诱导的肺泡巨噬细胞中NF-κB和C/EBP活性。此外，AT-RvD 1显著降低IgG IC刺激的肺泡巨噬细胞或中性粒细胞分泌TNF-α、IL-6、KC和MIP-1α。这些结果提示了阻断IC诱导的炎症的新方法。
Increasing evidence suggests that the novel anti-inflammatory and pro-resolving mediators such as the resolvins play an important role during inflammation. However, the functions of these lipid mediators in immune complex (IC)-induced lung injury remain unknown. Here, we determined the role of aspirin-triggered resolvin D1 (AT-RvD1) and its metabolically stable analogue, 17R-hydroxy-19-para-fluorophenoxy-resolvin D1 methyl ester (p-RvD1), in IgG IC-induced inflammatory responses in myeloid cells and injury in the lung. We show that lung vascular permeability in the AT-RvD1- or p-RvD1-treated mice were significantly reduced when compared with values in mice receiving control vesicle during the injury. Furthermore, i.v. administration of either AT-RvD1 or p-RvD1 caused significant decreases in the bronchoalveolar lavage fluids (BALF) contents of neutrophils, inflammatory cytokines, and chemokines. Of interest, AT-RvD1 or p-RvD1 significantly reduced BALF complement C5a level. By Electrophoretic Mobility Shift Assay, we demonstrate that IgG IC-induced activation of NF-κB and C/EBPβ transcription factors in the lung were significantly inhibited by AT-RvD1 and p-RvD1. Moreover, AT-RvD1 dramatically mitigates IgG IC-induced NF-κB and C/EBP activity in alveolar macrophages. Also, secretion of TNF-α, IL-6, KC, and MIP-1α from IgG IC-stimulated alveolar macrophages or neutrophils was significantly decreased by AT-RvD1. These results suggest a new approach to the blocking of IC-induced inflammation.
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影响因子：
32.4
作者：
Li, Yongsheng;Dalli, Jesmond;Chiang, Nan;Baron, Rebecca M.;Quintana, Carolina;Serhan, Charles N.
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DOI：
10.1161/atvbaha.112.249508
发表时间：
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影响因子：
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