Many studies have shown that adiponectin is closely related to chronic obstructive pulmonary disease (COPD), but the specific role of adiponectin in COPD is still not well understood. Adiponectin and IL‐6 expression in patients with acute exacerbation of COPD (AECOPD) was detected by ELISA. Human bronchial epithelial cells (HBECs) were stimulated with TNF‐α, IL‐6, apoptotic cells or LPS. Then, the expression of adiponectin was detected by qRT‐PCR and western blotting, and pro‐ and anti‐inflammatory factors were detected by ELISA. Adiponectin expression in AECOPD patients increased after treatment. TNF‐α and apoptotic cells promoted adiponectin expression in HBECs in a dose‐dependent manner, and apoptotic cells significantly promoted adiponectin secretion. IL‐6 also promoted adiponectin expression, but it inhibited adiponectin expression at high doses and with long treatment times. LPS inhibited adiponectin expression, but when HBECs were pretreated with anti‐TNF‐α and then treated with LPS, the expression and secretion of adiponectin increased significantly with increasing anti‐TNF‐α concentrations. Adiponectin stimulated the secretion of pro‐inflammatory factors in HBECs, but this effect was not concentration dependent. Adiponectin promoted the secretion of anti‐inflammatory factors in a dose‐dependent manner. Although LPS also stimulated HBECs to secrete pro‐inflammatory and anti‐inflammatory factors, adiponectin inhibited LPS‐induced pro‐inflammatory factor secretion and enhanced anti‐inflammatory factor secretion. Many factors regulate the expression and secretion of adiponectin, and adiponectin regulates the balance of the inflammatory response and inhibits further expansion of inflammation.

中文翻译：

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脂联素拮抗脂多糖调节气道上皮细胞中炎性因子的分泌，其表达受多种因素调节

许多研究表明，脂联素与慢性阻塞性肺疾病（COPD）密切相关，但脂联素在COPD中的具体作用仍未得到很好的了解。ELISA检测了COPD急性加重（AECOPD）患者的脂联素和IL-6表达。TNF-α，IL-6，凋亡细胞或LPS刺激人支气管上皮细胞（HBEC）。然后，通过qRT-PCR和western blotting检测脂联素的表达，并通过ELISA检测促炎和抗炎因子。治疗后AECOPD患者的脂联素表达增加。TNF-α和凋亡细胞以剂量依赖方式促进HBEC中脂联素的表达，凋亡细胞显着促进脂联素的分泌。IL-6也促进脂联素表达，但它在高剂量和长时间治疗下会抑制脂联素的表达。LPS抑制了脂联素的表达，但先用抗TNF-α预处理HBEC，然后再用LPS处理，脂联素的表达和分泌随抗TNF-α浓度的增加而显着增加。脂联素刺激了HBECs中促炎因子的分泌，但这种作用不是浓度依赖性的。脂联素以剂量依赖性方式促进抗炎因子的分泌。尽管脂多糖还刺激HBEC分泌促炎和抗炎因子，但脂连蛋白抑制脂多糖诱导的促炎因子分泌并增强了抗炎因子的分泌。许多因素调节脂联素的表达和分泌，