Anti-inflammatory effects of azithromycin in cystic fibrosis airway epithelial cells

Biochem Biophys Res Commun. 2006 Dec 1;350(4):977-82. doi: 10.1016/j.bbrc.2006.09.132. Epub 2006 Oct 2.


We aimed at identifying molecular mechanisms for anti-inflammatory effects of azithromycin (AZM) suggested by clinical evidences. IL-8 expression and DNA binding activity of two key pro-inflammatory transcription factors (TF), NF-kappaB and AP-1, were investigated in cystic fibrosis (CF) and isogenic non-CF airway epithelial cell lines. AZM reduced about 40% of IL-8 mRNA and protein expression (n=9, p=0.02, and n=4, p=0.00011) in CF cells reaching the levels of non-CF cells. In the presence of AZM we found about 50% and 70% reduction of NF-kappaB and AP-1 DNA binding, respectively (n=3, p=0.01, and n=3, p=0.0017), leading to levels of non-CF cells. The relevance of NF-kappaB and AP-1 in regulating IL-8 promoter transcriptional activity was demonstrated by gene reporter assays (n=4, p=8.54x10(-7), and n=4, p=6.45x10(-6)). Our data support the anti-inflammatory effects of AZM in CF cells, indicating inhibition of transcription of pro-inflammatory genes as possible mechanism, thus providing a rationale for the possible use of specific TF inhibitors for therapy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anti-Bacterial Agents / administration & dosage
  • Anti-Inflammatory Agents / administration & dosage
  • Azithromycin / administration & dosage*
  • Cell Line
  • Cystic Fibrosis / drug therapy
  • Cystic Fibrosis / metabolism*
  • Cystic Fibrosis / pathology*
  • Dose-Response Relationship, Drug
  • Epithelial Cells / drug effects
  • Epithelial Cells / metabolism*
  • Humans
  • Interleukin-8 / metabolism*
  • NF-kappa B / metabolism*
  • Transcription Factor AP-1 / metabolism*


  • Anti-Bacterial Agents
  • Anti-Inflammatory Agents
  • Interleukin-8
  • NF-kappa B
  • Transcription Factor AP-1
  • Azithromycin