Effects of Rhinovirus Infection on the Adherence ofStreptococcus pneumoniaeto Cultured Human Airway Epithelial Cells
Author(s) -
Satoshi Ishizuka,
Mutsuo Yamaya,
Tomoko Suzuki,
Hidenori Takahashi,
Shiroh IDA,
T. Sasaki,
Daisuke Inoue,
Kiyohisa Sekizawa,
Hidekazu Nishimura,
Hidetada Sasaki
Publication year - 2003
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/379833
Subject(s) - rhinovirus , streptococcus pneumoniae , pyrrolidine dithiocarbamate , biology , microbiology and biotechnology , platelet activating factor receptor , respiratory epithelium , immunology , epithelium , receptor , inflammation , nf κb , virus , antagonist , antibiotics , biochemistry , genetics
To examine the effects of rhinovirus (RV) infection on the adherence of Streptococcus pneumoniae to human tracheal epithelial cells, cells were infected with RV-14, and S. pneumoniae were added to the culture medium. The number of S. pneumoniae adhering to epithelial cells increased after RV infection. Y-24180, a specific inhibitor of the platelet-activating factor receptor (PAF-R); PAF; and the pyrrolidine derivative of dithiocarbamate, an inhibitor of transcription factor nuclear factor-kappaB (NF-kappaB), decreased the number of S. pneumoniae adhering to cells after RV-14 infection. RV-14 infection increased PAF-R expression and the activation of NF-kappaB and promoter-specific transcription factor 1. These findings suggest that RV-14 infection stimulates S. pneumoniae adhesion to airway epithelial cells via increases in PAF-Rs that are partly mediated through activation of transcription factors. Increased adherence of S. pneumoniae may be one of the reasons that pneumonia develops after RV infection.
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