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Long-term azithromycin in cystic fibrosis: another possible mechanism of action?

U Pradal1, A Delmarco, M Morganti

  • 1Cystic Fibrosis Center, Azienda Ospedaliera di Verona, Verona, Italy. ugo.pradal@azosp.vr.it

Journal of Chemotherapy (Florence, Italy)
|September 20, 2005
PubMed

Insights

Azithromycin treatment improved chloride transport in cystic fibrosis patients by potentially increasing multidrug resistance-associated protein (MRP) expression. This suggests a new therapeutic role for azithromycin in managing cystic fibrosis lung disease.

Area of Science:

  • Pulmonary Medicine
  • Pharmacology
  • Genetics

Background:

  • Azithromycin is used for cystic fibrosis (CF) lung disease, but its exact mechanisms are unclear.
  • Potential mechanisms include anti-inflammatory, antimicrobial effects, or modulation of ion transport via multidrug resistance-associated protein (MRP).

Purpose of the Study:

  • To investigate if azithromycin treatment in CF patients affects ion transport and MRP expression.
  • To explore a novel therapeutic role for azithromycin in CF.

Main Methods:

  • Seven CF patients received azithromycin (500 mg daily) for 4 weeks.
  • Nasal potential difference (NPD) measured in vivo for ion transport.
  • Semi-quantitative RT-PCR assessed MRP mRNA expression in nasal cells.

Main Results:

  • NPD indicated impaired sodium transport but significantly increased chloride conductance post-treatment (p=0.03).
  • MRP mRNA expression significantly correlated with improved chloride conductance (p=0.04, r=0.78).

Conclusions:

  • Azithromycin may induce MRP overexpression, restoring chloride conductance in CF airways.
  • This suggests azithromycin could offer a new therapeutic strategy for CF pulmonary disease by compensating for the ion transport defect.

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