Abstract：
Smoking causes several diseases such as chronic obstructive pulmonary disease (COPD). Aspirin-triggered-resolvin D1 (AT-RvD1) is a lipid mediator produced during the resolution of inflammation and demonstrates anti-inflammatory and pro-resolution effects in several inflammatory experimental models including in the airways. Here we evaluated the role of AT-RvD1 (100 nM) in bronchial epithelial cells (BEAS-2B) stimulated by cigarette smoke extract (CSE; 1%; 1 cigarette) for 24 h. CSE induced the productions of IL-1β, TNF-α, IL-10, IL-4 and IFN-γ as well as the activations of NF-κB and STAT3 and the expression of ALX/FPR2 receptor. AT-RvD1 reduced the IL-1β and TNF-α production and increased the production of IFN-γ. These effects were reversed BOC2, an antagonist of ALX/FPR2 receptor for AT-RvD1. The production of IL-4 and IL-10 were not altered by AT-RvD1. In addition, AT-RvD1 reduced the phosphorylation of NF-κB and STAT3 when compared to CSE-stimulated BEAS-2B cells. No alteration of ALX/FPR2 expression was observed by AT-RvD1 when compared to CSE group. In the human monocytic leukemia cell line, the relative number of copies of IL-1β and IL-4 was significantly higher in CSE + AT-RvD1 group compared CSE group, however, the expression of M1 cytokine was more pronounced than M2 profile. AT-RvD1 could be an important target for the reduction of inflammation in the airways associated with smoking.
摘要：
吸烟会导致多种疾病，例如慢性阻塞性肺疾病（COPD）。阿司匹林触发的消退素D1（AT-RvD1）是在炎症消退过程中产生的脂质介质，并在包括气道在内的几种炎症实验模型中显示出抗炎和促消退作用。在这里，我们评估了AT-RvD1（100nM）在香烟烟雾提取物（CSE；1％；1支香烟）刺激24小时的支气管上皮细胞（BEAS-2B）中的作用。CSE诱导IL-1β的产生，TNF-α,IL-10，IL-4和IFN-γ以及NF-κB和STAT3的激活以及ALX/FPR2受体的表达。AT-RvD1减少IL-1β和TNF-α的产生并增加IFN-γ的产生。这些作用被逆转了BOC2，一种AT-RvD1的ALX/FPR2受体拮抗剂。AT-RvD1没有改变IL-4和IL-10的产生。此外,与CSE刺激的BEAS-2B细胞相比，AT-RvD1降低了NF-κB和STAT3的磷酸化。当与CSE组比较时,通过AT-RvD1没有观察到ALX/FPR2表达的改变。在人类单核细胞白血病细胞系中，CSE+AT-RvD1组IL-1β和IL-4的相对拷贝数明显高于CSE组,然而,M1细胞因子的表达比M2更明显。AT-RvD1可能是减少与吸烟相关的气道炎症的重要靶标。
