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首页> 外文期刊>The journal of immunology >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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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

机译：阿司匹林引发的（17R）Resolvin D1及其类似物17R-羟基-19-巴拉-氟苯氧基-Resolvin D1甲基酯在C5a依赖性IgG免疫复合物诱导的炎症和肺损伤中的保护作用。

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Increasing evidence suggests that the novel anti-inflammatory and proresolving mediators such as the resolvins play an important role during inflammation. However, the functions of these lipid mediators in immune complex–induced lung injury remain unknown. In this study, we determined the role of aspirin-triggered resolvin D1 (AT-RvD1) and its metabolically stable analog, 17R-hydroxy-19- para -fluorophenoxy-resolvin D1 methyl ester (p-RvD1), in IgG immune complex–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 was 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 fluid contents of neutrophils, inflammatory cytokines, and chemokines. Of interest, AT-RvD1 or p-RvD1 significantly reduced bronchoalveolar lavage fluid complement C5a level. By EMSA, we demonstrate that IgG immune complex–induced activation of NF-κB and C/EBPβ transcription factors in the lung was significantly inhibited by AT-RvD1 and p-RvD1. Moreover, AT-RvD1 dramatically mitigates IgG immune complex–induced NF-κB and C/EBP activity in alveolar macrophages. Also, secretion of TNF-α, IL-6, keratinocyte cell–derived chemokine, and MIP-1α from IgG immune complex–stimulated alveolar macrophages or neutrophils was significantly decreased by AT-RvD1. These results suggest a new approach to the blocking of immune complex–induced inflammation.
机译：越来越多的证据表明，新型的消炎和能解决炎症的介质（例如，RESOLVIN）在炎症过程中起着重要的作用。但是，这些脂质介体在免疫复合物诱导的肺损伤中的功能仍然未知。在这项研究中，我们确定了阿司匹林触发的resolvin D1（AT-RvD1）及其代谢稳定的类似物17R-羟基-19-对氟苯氧基-resolvin D1甲基酯（p-RvD1）在IgG免疫复合物中的作用–引起髓样细胞的炎症反应和肺损伤。我们显示，与损伤期间接受对照囊泡的小鼠相比，AT-RvD1–或p-RvD1–治疗的小鼠的肺血管通透性显着降低。此外，i.v。施用AT-RvD1或p-RvD1会导致嗜中性粒细胞，炎性细胞因子和趋化因子的支气管肺泡灌洗液含量显着降低。有趣的是，AT-RvD1或p-RvD1显着降低了支气管肺泡灌洗液补体C5a的水平。通过EMSA，我们证明AT-RvD1和p-RvD1显着抑制IgG免疫复合物诱导的肺中NF-κB和C /EBPβ转录因子的激活。此外，AT-RvD1可以显着减轻IgG免疫复合物诱导的肺泡巨噬细胞中NF-κB和C / EBP的活性。此外，AT-RvD1可以显着减少IgG免疫复合物刺激的肺泡巨噬细胞或中性粒细胞分泌TNF-α，IL-6，角质形成细胞衍生的趋化因子和MIP-1α。这些结果表明了一种阻止免疫复合物诱导的炎症的新方法。

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