Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, PR China.
Department of Immunology, College of Basic Medicine, Chongqing Medical University, Chongqing 400016, PR China.
Cytokine. 2020 Sep;133:155148. doi: 10.1016/j.cyto.2020.155148. Epub 2020 Jun 3.
Airway macrophages represents a central site for the mechanisms involved in the complex interactions between environmental triggers and airway inflammation. Based on anti-inflammatory activity of adiponectin, we hypothesize that adiponectin inhibits the proinflammatory cytokines production and the activation of alveolar macrophages expose to cigarette smoke.
To examine the effects of adiponectin on alveolar macrophages, we used the cigarette smoke-induced the alveolar inflammation model in C57BL/6 mice and the macrophages activation model in vitro, both in the presence or absence of adiponectin, to assess the accumulation of inflammatory cells and the concentration of inflammatory cytokines and chemokines in the bronchoalveolar lavage (BAL), and the proinflammatory cytokines production and M1/2 phenotype in alveolar macrophages.
Our results showed that adiponectin improves cigarette smoke-induced airway inflammation in vivo and decreases proinflammatory cytokine production and alveolar macrophages polarization in vitro. Moreover, our study further demonstrates that anti-inflammatory activity of adiponectin depends on the suppression of the proinflammatory cytokine production through TLR2/4 signaling and the inhibition of macrophage polarization vit COX-2/PGE2 signaling.
Our study suggests that the anti-inflammatory activity of adiponectin might contribute to its therapeutic potential in airway inflammation, such as COPD.
气道巨噬细胞代表了参与环境触发因素与气道炎症之间复杂相互作用的机制的中心部位。基于脂联素的抗炎活性，我们假设脂联素抑制促炎细胞因子的产生，并抑制暴露于香烟烟雾的肺泡巨噬细胞的激活。
为了研究脂联素对肺泡巨噬细胞的影响，我们使用香烟烟雾诱导的 C57BL/6 小鼠肺泡炎症模型和体外巨噬细胞激活模型，在存在或不存在脂联素的情况下，评估炎症细胞的积聚和支气管肺泡灌洗液（BAL）中炎症细胞因子和趋化因子的浓度，以及肺泡巨噬细胞中促炎细胞因子的产生和 M1/2 表型。
我们的结果表明，脂联素改善了体内香烟烟雾诱导的气道炎症，并减少了体外促炎细胞因子的产生和肺泡巨噬细胞的极化。此外，我们的研究进一步表明，脂联素的抗炎活性取决于通过 TLR2/4 信号抑制促炎细胞因子的产生，以及通过 COX-2/PGE2 信号抑制巨噬细胞极化。
我们的研究表明，脂联素的抗炎活性可能有助于其在气道炎症（如 COPD）中的治疗潜力。
