Department of Respiratory and Critical Care Medicine, Taizhou Clinical Medical School of Nanjing Medical University (Taizhou People's Hospital), Taizhou, China.
Department of Cardiology, Taizhou Clinical Medical School of Nanjing Medical University (Taizhou People's Hospital), Taizhou, China.
J Clin Lab Anal. 2021 Jul;35(7):e23857. doi: 10.1002/jcla.23857. Epub 2021 Jun 7.
Smoking is likely to facilitate airway inflammation and finally contributes to chronic obstructive pulmonary disease (COPD). This investigation was intended to elucidate miRNAs that were involved in smoking-induced COPD.
Altogether 155 COPD patients and 77 healthy volunteers were recruited, and their serum levels of miR-221-3p and miR-92a-3p were determined. Besides, human bronchial epithelial cells (16HBECs) were purchased, and they were treated by varying concentrations of cigarette smoke extract (CSE). The 16HBECs were, additionally, transfected by miR-221-3p mimic, miR-92a-3p mimic, miR-221-3p inhibitor or miR-92a-3p inhibitor, and cytokines released by them, including TNF-α, IL-8, IL-1β, and TGF-β1, were monitored using enzyme linked immunosorbent assay (ELISA) kits.
Chronic obstructive pulmonary disease patients possessed higher serum levels of miR-221-3p and miR-92a-3p than healthy volunteers (p < 0.05), and both miR-221-3p and miR-92a-3p were effective biomarkers in diagnosing stable COPD from acute exacerbation COPD. Moreover, viability of 16HBECs was undermined by CSE treatment (p < 0.05), and exposure to CSE facilitated 16HBECs' release of TNF-α, IL-8, IL-1β, and TGF-β1 (p < 0.05). Furthermore, miR-221-3p/miR-92a-3p expression in 16HBECs was significantly suppressed after transfection of miR-221-3p/miR-92a-3p inhibitor (p < 0.05), which abated CSE-triggered increase in cytokine production and decline in viability of 16HBECs (p < 0.05).
MiR-221-3p and miR-92a-3p were involved in CSE-induced hyperinflammation of COPD, suggesting that they were favorable alternatives in diagnosing COPD patients with smoking history.
吸烟可能促进气道炎症，最终导致慢性阻塞性肺疾病（COPD）。本研究旨在阐明参与吸烟诱导的 COPD 的 miRNA。
共招募了 155 例 COPD 患者和 77 例健康志愿者，并测定其血清 miR-221-3p 和 miR-92a-3p 水平。此外，还购买了人支气管上皮细胞（16HBEC），并用不同浓度的香烟烟雾提取物（CSE）处理。还将 miR-221-3p 模拟物、miR-92a-3p 模拟物、miR-221-3p 抑制剂或 miR-92a-3p 抑制剂转染 16HBEC，并用酶联免疫吸附试验（ELISA）试剂盒监测它们释放的细胞因子，包括 TNF-α、IL-8、IL-1β 和 TGF-β1。
COPD 患者的血清 miR-221-3p 和 miR-92a-3p 水平高于健康志愿者（p<0.05），miR-221-3p 和 miR-92a-3p 是稳定型 COPD 从急性加重型 COPD 诊断的有效生物标志物。此外，CSE 处理会降低 16HBEC 的活力（p<0.05），并且暴露于 CSE 会促进 16HBEC 释放 TNF-α、IL-8、IL-1β 和 TGF-β1（p<0.05）。此外，转染 miR-221-3p/miR-92a-3p 抑制剂后，16HBEC 中的 miR-221-3p/miR-92a-3p 表达明显受到抑制（p<0.05），减弱了 CSE 引起的细胞因子产生增加和 16HBEC 活力下降（p<0.05）。
miR-221-3p 和 miR-92a-3p 参与了 CSE 诱导的 COPD 过度炎症反应，提示它们是诊断有吸烟史的 COPD 患者的有利选择。
