<p>We investigated serum miR-155 in chronic obstructive pulmonary disease (COPD) and its clinical utility. miR-155 in peripheral blood mononuclear cells (PBMCs) and serum cytokines (IL-1β, IL-6, IL-8, TNF-α) were quantified, and associations with disease occurrence, inflammation, severity, and prognosis were assessed over one year. A total of 117 participants were enrolled: 59 COPD patients (29 acute exacerbation [AECOPD], 30 stable), 31 heavy smokers, and 27 healthy controls. miR-155 was measured by RT-PCR and cytokines by ELISA. COPD patients were prospectively followed and categorized as frequent exacerbators (FE) or non-frequent exacerbators (NFE) to evaluate miR-155’s predictive value. miR-155 was significantly elevated in COPD and heavy-smoking groups versus controls (<i>P</i> &lt; 0.01) and higher in AECOPD than stable COPD (<i>P</i> &lt; 0.01). ROC analysis identified optimal cutoff 0.578 (sensitivity 68.97%, specificity 96.67%, AUC = 0.8724). In AECOPD, miR-155 was lower in invasive pulmonary aspergillosis (IPA) than non-IPA patients (<i>P</i> &lt; 0.01). All inflammatory cytokines were significantly elevated in AECOPD versus other groups (<i>P</i> &lt; 0.01). miR-155 showed positive correlations with IL-1β (<i>R</i> = 0.22, 95% CI 0.03–0.39, <i>P</i> &lt; 0.05), IL-6 (<i>R</i> = 0.20, 95% CI 0.01–0.37, <i>P</i> &lt; 0.05), IL-8 (<i>R</i> = 0.20, 95% CI 0.02–0.37, <i>P</i> &lt; 0.05), TNF-α (<i>R</i> = 0.22, 95% CI 0.04–0.39, <i>P</i> &lt; 0.05), GOLD stage (<i>R</i> = 0.35, 95% CI 0.10–0.55, <i>P</i> &lt; 0.01), and ABE grouping (<i>R</i> = 0.66, 95% CI 0.49–0.79, <i>P</i> &lt; 0.01). FE patients had higher miR-155 than NFE (<i>P</i> &lt; 0.001), with moderate correlation to exacerbation frequency (<i>R</i> = 0.63, 95% CI 0.45–0.76, <i>P</i> &lt; 0.01). miR-155 is involved in smoking-related COPD pathogenesis and shows promise as a biomarker for identifying AECOPD and differentiating IPA from non-IPA infections. Its correlations with inflammatory cytokines and disease severity support its utility in assessing inflammatory burden and clinical severity. Elevated miR-155 predicts frequent exacerbations, highlighting its potential as a prognostic biomarker.</p>

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Diagnostic and prognostic value of serum miR-155 in chronic obstructive pulmonary disease

  • Yongming Wu,
  • Kaijun Zhang,
  • Rongrong Zhong,
  • Weihong Wang,
  • Zhaodi Luo,
  • Zhiyi Ma,
  • Rongzhang Liang,
  • Xiaoming Wu,
  • Xin Zou

摘要

We investigated serum miR-155 in chronic obstructive pulmonary disease (COPD) and its clinical utility. miR-155 in peripheral blood mononuclear cells (PBMCs) and serum cytokines (IL-1β, IL-6, IL-8, TNF-α) were quantified, and associations with disease occurrence, inflammation, severity, and prognosis were assessed over one year. A total of 117 participants were enrolled: 59 COPD patients (29 acute exacerbation [AECOPD], 30 stable), 31 heavy smokers, and 27 healthy controls. miR-155 was measured by RT-PCR and cytokines by ELISA. COPD patients were prospectively followed and categorized as frequent exacerbators (FE) or non-frequent exacerbators (NFE) to evaluate miR-155’s predictive value. miR-155 was significantly elevated in COPD and heavy-smoking groups versus controls (P < 0.01) and higher in AECOPD than stable COPD (P < 0.01). ROC analysis identified optimal cutoff 0.578 (sensitivity 68.97%, specificity 96.67%, AUC = 0.8724). In AECOPD, miR-155 was lower in invasive pulmonary aspergillosis (IPA) than non-IPA patients (P < 0.01). All inflammatory cytokines were significantly elevated in AECOPD versus other groups (P < 0.01). miR-155 showed positive correlations with IL-1β (R = 0.22, 95% CI 0.03–0.39, P < 0.05), IL-6 (R = 0.20, 95% CI 0.01–0.37, P < 0.05), IL-8 (R = 0.20, 95% CI 0.02–0.37, P < 0.05), TNF-α (R = 0.22, 95% CI 0.04–0.39, P < 0.05), GOLD stage (R = 0.35, 95% CI 0.10–0.55, P < 0.01), and ABE grouping (R = 0.66, 95% CI 0.49–0.79, P < 0.01). FE patients had higher miR-155 than NFE (P < 0.001), with moderate correlation to exacerbation frequency (R = 0.63, 95% CI 0.45–0.76, P < 0.01). miR-155 is involved in smoking-related COPD pathogenesis and shows promise as a biomarker for identifying AECOPD and differentiating IPA from non-IPA infections. Its correlations with inflammatory cytokines and disease severity support its utility in assessing inflammatory burden and clinical severity. Elevated miR-155 predicts frequent exacerbations, highlighting its potential as a prognostic biomarker.