Institute of Health Sciences, Department of Clinical Medicine, Laboratory of Experimental Immunopharmacology, Federal University of Triângulo Mineiro, Uberaba, MG 38025-350, Brazil.
Laboratory of Immunology, Institute of Biological and Natural Sciences, Department of Microbiology, Immunology and Parasitology, Federal University of Triângulo Mineiro, Uberaba, Minas Gerais, Brazil.
Prostaglandins Other Lipid Mediat. 2024 Jun;172:106833. doi: 10.1016/j.prostaglandins.2024.106833. Epub 2024 Mar 7.
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.
吸烟可导致多种疾病，如慢性阻塞性肺疾病（COPD）。阿司匹林触发的 resolvin D1（AT-RvD1）是一种在炎症消退过程中产生的脂质介质，在包括气道在内的几种炎症实验模型中具有抗炎和促消退作用。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）刺激的支气管上皮细胞（BEAS-2B）中 24 小时的作用。CSE 诱导了 IL-1β、TNF-α、IL-10、IL-4 和 IFN-γ的产生，以及 NF-κB 和 STAT3 的激活和 ALX/FPR2 受体的表达。AT-RvD1 降低了 IL-1β和 TNF-α的产生，增加了 IFN-γ的产生。这些作用被 BOC2 逆转，BOC2 是 AT-RvD1 对 ALX/FPR2 受体的拮抗剂。AT-RvD1 对 IL-4 和 IL-10 的产生没有影响。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。与 CSE 组相比，AT-RvD1 对 ALX/FPR2 表达没有改变。在人单核白血病细胞系中，与 CSE 组相比，CSE+AT-RvD1 组的 IL-1β 和 IL-4 的相对拷贝数明显更高，但 M1 细胞因子的表达比 M2 谱更明显。AT-RvD1 可能是减少与吸烟相关的气道炎症的一个重要靶点。
