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Rhinovirus enhances various bacterial adhesions to nasal epithelial cells simultaneously

Authors

  • Jong Hwan Wang MD,

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

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

    Corresponding author
    1. Department of Otolaryngology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea
    • Department of Otolaryngology, Asan Medical Center, University of Ulsan College of Medicine, Pungnap-2dong, Songpa-gu, Seoul, Korea
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Abstract

Objectives/Hypothesis:

Viral upper respiratory tract infections are often followed by secondary bacterial infections in the form of acute rhinosinusitis. We investigate the effect of rhinovirus infection on the expression of cell adhesion molecules and bacterial adherence to primary human nasal epithelial cells.

Methods:

Cells were infected with rhinovirus serotype 16 (RV-16), and then Staphylococcus aureus, Streptococcus pneumoniae, or Hemophilus influenzae were added to the culture. Rhinovirus-induced expression of fibronectin, platelet-activating factor receptor, and carcinoembryonic antigen-related cell adhesion molecule, was assayed by confocal microscopy, real-time polymerase chain reaction, and Western blot analysis. Bacterial adhesion to cells was assessed by confocal microscopy and the fluorescence intensity of adherent bacteria was analyzed using Image-Pro Plus 5.1 (Media Cybernetics, Inc., Bethesda, MD).

Results:

RV-16 infection significantly increased the gene and protein expression of fibronectin, platelet-activating factor receptor, and carcinoembryonic antigen-related cell adhesion molecule in nasal epithelial cells. Compared with rhinovirus-uninfected control cells, the adhesion of S. aureus, S. pneumoniae, and H. influenzae increased significantly to 2.53-fold, 1.51-fold, and 2.74-fold of control levels, respectively, in rhinovirus-infected nasal epithelial cells.

Conclusions:

These findings suggest that increased expression of host cell adhesion molecules may be the mechanism accounting for the increase in susceptibility to bacterial rhinosinusitis associated with rhinovirus-induced upper respiratory infections. Laryngoscope, 2009

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