The expression of Mirc1/Mir17-92 cluster in sputum samples correlates with pulmonary exacerbations in cystic fibrosis patients

J Cyst Fibros. 2018 Jul;17(4):454-461. doi: 10.1016/j.jcf.2017.11.005. Epub 2017 Dec 11.

Abstract

Introduction: Cystic fibrosis (CF) is a multi-organ disorder characterized by chronic sino-pulmonary infections and inflammation. Many patients with CF suffer from repeated pulmonary exacerbations that are predictors of worsened long-term morbidity and mortality. There are no reliable markers that associate with the onset or progression of an exacerbation or pulmonary deterioration. Previously, we found that the Mirc1/Mir17-92a cluster which is comprised of 6 microRNAs (Mirs) is highly expressed in CF mice and negatively regulates autophagy which in turn improves CF transmembrane conductance regulator (CFTR) function. Therefore, here we sought to examine the expression of individual Mirs within the Mirc1/Mir17-92 cluster in human cells and biological fluids and determine their role as biomarkers of pulmonary exacerbations and response to treatment.

Methods: Mirc1/Mir17-92 cluster expression was measured in human CF and non-CF plasma, blood-derived neutrophils, and sputum samples. Values were correlated with pulmonary function, exacerbations and use of CFTR modulators.

Results: Mirc1/Mir17-92 cluster expression was not significantly elevated in CF neutrophils nor plasma when compared to the non-CF cohort. Cluster expression in CF sputum was significantly higher than its expression in plasma. Elevated CF sputum Mirc1/Mir17-92 cluster expression positively correlated with pulmonary exacerbations and negatively correlated with lung function. Patients with CF undergoing treatment with the CFTR modulator Ivacaftor/Lumacaftor did not demonstrate significant change in the expression Mirc1/Mir17-92 cluster after six months of treatment.

Conclusions: Mirc1/Mir17-92 cluster expression is a promising biomarker of respiratory status in patients with CF including pulmonary exacerbation.

Keywords: Biomarker; Correlation; Cystic fibrosis; MicroRNA; Mir17–92a; Pulmonary exacerbation.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Aminophenols / administration & dosage*
  • Aminopyridines / administration & dosage*
  • Benzodioxoles / administration & dosage*
  • Biomarkers / metabolism
  • Chloride Channel Agonists / administration & dosage
  • Correlation of Data
  • Cystic Fibrosis Transmembrane Conductance Regulator / genetics
  • Cystic Fibrosis* / drug therapy
  • Cystic Fibrosis* / genetics
  • Cystic Fibrosis* / metabolism
  • Cystic Fibrosis* / physiopathology
  • Disease Progression
  • Drug Combinations
  • Drug Monitoring / methods
  • Female
  • Gene Expression Profiling
  • Humans
  • Male
  • MicroRNAs / metabolism*
  • Nerve Tissue Proteins / metabolism*
  • Quinolones / administration & dosage*
  • RNA, Long Noncoding
  • Respiratory Function Tests / methods
  • Respiratory System* / drug effects
  • Respiratory System* / metabolism
  • Respiratory System* / physiopathology
  • Sputum / metabolism

Substances

  • Aminophenols
  • Aminopyridines
  • Benzodioxoles
  • Biomarkers
  • CFTR protein, human
  • Chloride Channel Agonists
  • Drug Combinations
  • FSD1 protein, human
  • MIR17HG, human
  • MicroRNAs
  • Nerve Tissue Proteins
  • Quinolones
  • RNA, Long Noncoding
  • lumacaftor, ivacaftor drug combination
  • Cystic Fibrosis Transmembrane Conductance Regulator