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Absorption of Nasal and Bronchial Fluids: Precision Sampling of the Human Respiratory Mucosa and Laboratory Processing of Samples
11:54

Absorption of Nasal and Bronchial Fluids: Precision Sampling of the Human Respiratory Mucosa and Laboratory Processing of Samples

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Clarithromycin inhibits rhinovirus-induced bacterial adhesions to nasal epithelial cells

Jong Hwan Wang1, Si Hyeong Lee, Hyun Ja Kwon

  • 1Department of Otolaryngology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea.

The Laryngoscope
|October 31, 2009
PubMed
Abstract

Insights

Clarithromycin (CM) prevents secondary bacterial infections in rhinovirus (RV)-infected cells. CM inhibits RV-induced fibronectin and CEACAMs, reducing Staphylococcus aureus and Haemophilus influenzae adhesion.

Area of Science:

  • Respiratory viral infections
  • Bacterial pathogenesis
  • Pharmacology

Background:

  • Rhinovirus (RV) infections can lead to secondary bacterial infections.
  • Fibronectin (Fn) and CEACAMs are key receptors for Staphylococcus aureus and Haemophilus influenzae.
  • Understanding host-pathogen interactions is crucial for preventing complications.

Purpose of the Study:

  • To investigate clarithromycin's (CM) inhibitory effects on RV-induced Fn and CEACAM expression.
  • To assess CM's impact on bacterial adhesion to RV-infected nasal epithelial cells.

Main Methods:

  • Primary human nasal epithelial cells (HNECs) were treated with CM before RV-16 infection.
  • Gene and protein expression of Fn and CEACAMs were analyzed using RT-PCR and Western blotting.
  • Bacterial adhesion assays were performed using confocal microscopy.

Main Results:

  • CM significantly inhibited RV-induced Fn and CEACAM gene and protein expression in HNECs.
  • CM treatment markedly reduced S. aureus and H. influenzae adhesion to RV-infected HNECs.
  • Bacterial adhesion levels in CM-treated cells returned to those of non-infected controls.

Conclusions:

  • Clarithromycin demonstrates potential in preventing secondary bacterial infections following RV infection.
  • CM acts by inhibiting Fn and CEACAM expression, thereby reducing bacterial adherence.
  • This mechanism highlights CM's role in managing complex respiratory infections.

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