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Background <p>Non–cystic fibrosis bronchiectasis (NCFB) is a chronic respiratory condition characterized by irreversible bronchial dilatation and persistent inflammation. Although inflammation plays a central role in disease progression, the upstream regulatory mechanisms remain incompletely understood. MicroRNA-155 (miR-155) is a well-recognized modulator of immune responses in chronic lung diseases, but its role in NCFB has not been previously elucidated.</p> Methods <p><?tk 2?>This study enrolled 58 NCFB patients and 30 healthy controls. The expression of miR-155 in peripheral blood mononuclear cells (PBMC) was quantified using qRT-PCR. Serum levels of IL-1β, IL-6, IL-8, and TNF-α were assessed by ELISA. Correlations between miR-155 expression and inflammatory cytokines, clinical indices, and <i>Pseudomonas aeruginosa</i> colonization were evaluated. In vitro, BEAS-2B epithelial cells were transfected with miR-155 mimics or inhibitors, and cytokine production was measured following LPS stimulation.</p> Results <p>MiR-155 expression was significantly elevated in NCFB patients and positively correlated with IL-6, IL-8, TNF-α, and IL-1β levels (all <i>p</i> &lt; 0.01). Higher miR-155 expression was also associated with increased disease burden, including elevated BSI scores and <i>P. aeruginosa</i> colonization. In vitro, miR-155 overexpression in BEAS-2B cells markedly enhanced pro-inflammatory cytokine secretion upon LPS stimulation, while inhibition of miR-155 suppressed cytokine release.</p> Conclusion <p>miR-155 is upregulated in NCFB and closely associated with systemic and airway inflammation. It actively promotes pro-inflammatory signaling in airway epithelial cells, suggesting a pathogenic role in sustaining chronic inflammation. These findings highlight miR-155 as a potential biomarker of disease activity and a candidate target for immune modulation in bronchiectasis.</p>

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Diagnostic and prognostic value of miR-155 in non–cystic fibrosis bronchiectasis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月11日

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  • Wenying Li,
  • Xingbin Yu,
  • Weihong Wang,
  • Rongzhang Liang,
  • Zhaodi Luo,
  • Xin Zou,
  • Liwen Lin,
  • Kaijun Zhang,
  • Yongming Wu

摘要

Background

Non–cystic fibrosis bronchiectasis (NCFB) is a chronic respiratory condition characterized by irreversible bronchial dilatation and persistent inflammation. Although inflammation plays a central role in disease progression, the upstream regulatory mechanisms remain incompletely understood. MicroRNA-155 (miR-155) is a well-recognized modulator of immune responses in chronic lung diseases, but its role in NCFB has not been previously elucidated.

Methods

This study enrolled 58 NCFB patients and 30 healthy controls. The expression of miR-155 in peripheral blood mononuclear cells (PBMC) was quantified using qRT-PCR. Serum levels of IL-1β, IL-6, IL-8, and TNF-α were assessed by ELISA. Correlations between miR-155 expression and inflammatory cytokines, clinical indices, and Pseudomonas aeruginosa colonization were evaluated. In vitro, BEAS-2B epithelial cells were transfected with miR-155 mimics or inhibitors, and cytokine production was measured following LPS stimulation.

Results

MiR-155 expression was significantly elevated in NCFB patients and positively correlated with IL-6, IL-8, TNF-α, and IL-1β levels (all p < 0.01). Higher miR-155 expression was also associated with increased disease burden, including elevated BSI scores and P. aeruginosa colonization. In vitro, miR-155 overexpression in BEAS-2B cells markedly enhanced pro-inflammatory cytokine secretion upon LPS stimulation, while inhibition of miR-155 suppressed cytokine release.

Conclusion

miR-155 is upregulated in NCFB and closely associated with systemic and airway inflammation. It actively promotes pro-inflammatory signaling in airway epithelial cells, suggesting a pathogenic role in sustaining chronic inflammation. These findings highlight miR-155 as a potential biomarker of disease activity and a candidate target for immune modulation in bronchiectasis.