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Polyinosine-polycytidylic acid enhances cellular adherence of Streptococcus pneumoniae

Authors

  • Masaki Kawabata MD,

    Corresponding author
    1. Department of Otolaryngology–Head and Neck Surgery, Kagoshima University, Graduate School of Medical and Dental Science, Kagoshima, Japan
    • Department of Otolaryngology, Head and Neck Surgery, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1, Kagoshima 890-8520, Japan
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  • Yuichi Kurono MD

    1. Department of Otolaryngology–Head and Neck Surgery, Kagoshima University, Graduate School of Medical and Dental Science, Kagoshima, Japan
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  • The authors have no funding, financial relationships, or conflicts of interest to disclose.

Abstract

Objectives/Hypothesis:

Viral upper respiratory tract infections (URIs) are often followed by secondary bacterial infections. To better understand this phenomenon, we examined the impact of the viral agent polyinosine-polycytidylic acid [Poly (I:C)] on the adherence of Streptococcus pneumoniae (Spn) to pharyngeal epithelial cells.

Study Design:

In vitro model of cultured human pharyngeal epithelial cells.

Methods:

Detroit 562 cells, a human pharyngeal carcinoma cell line, were pretreated with Poly (I:C). Poly (I:C)–induced expression of platelet-activating factor receptor (PAF-R) was assayed using real-time polymerase chain reaction, flow cytometry, and immunofluorescence microscopy. Bacterial adhesion to these epithelial cells was assessed using immunofluorescence microscopy and colony formation assays.

Results:

Pretreatment with Poly (I:C) increased mRNA and protein expression of PAF-R in Detroit 562 cells and enhanced the adherence of Spn to these epithelial cells.

Conclusions:

RNA viral infection can enhance PAF-R expression in epithelial cells and increase the adherence of Spn. These findings might explain in part the mechanisms that underlie the increase in bacterial infection following URIs.

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