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This investigation was intended to elucidate miRNAs that were involved in smoking\u2010induced COPD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Altogether 155 COPD patients and 77\u00a0healthy volunteers were recruited, and their serum levels of miR\u2010221\u20103p and miR\u201092a\u20103p 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\u2010221\u20103p mimic, miR\u201092a\u20103p mimic, miR\u2010221\u20103p inhibitor or miR\u201092a\u20103p inhibitor, and cytokines released by them, including TNF\u2010\u03b1, IL\u20108, IL\u20101\u03b2, and TGF\u2010\u03b21, were monitored using enzyme linked immunosorbent assay (ELISA) kits.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Chronic obstructive pulmonary disease patients possessed higher serum levels of miR\u2010221\u20103p and miR\u201092a\u20103p than healthy volunteers (\n                      <jats:italic>p<\/jats:italic>\n                      \u00a0&lt;\u00a00.05), and both miR\u2010221\u20103p and miR\u201092a\u20103p were effective biomarkers in diagnosing stable COPD from acute exacerbation COPD. Moreover, viability of 16HBECs was undermined by CSE treatment (\n                      <jats:italic>p<\/jats:italic>\n                      \u00a0&lt;\u00a00.05), and exposure to CSE facilitated 16HBECs\u2019 release of TNF\u2010\u03b1, IL\u20108, IL\u20101\u03b2, and TGF\u2010\u03b21 (\n                      <jats:italic>p<\/jats:italic>\n                      \u00a0&lt;\u00a00.05). Furthermore, miR\u2010221\u20103p\/miR\u201092a\u20103p expression in 16HBECs was significantly suppressed after transfection of miR\u2010221\u20103p\/miR\u201092a\u20103p inhibitor (\n                      <jats:italic>p<\/jats:italic>\n                      \u00a0&lt;\u00a00.05), which abated CSE\u2010triggered increase in cytokine production and decline in viability of 16HBECs (\n                      <jats:italic>p<\/jats:italic>\n                      \u00a0&lt;\u00a00.05).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>MiR\u2010221\u20103p and miR\u201092a\u20103p were involved in CSE\u2010induced hyperinflammation of COPD, suggesting that they were favorable alternatives in diagnosing COPD patients with smoking history.<\/jats:p>\n                  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