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Polyinosine-polycytidylic acid enhances cellular adherence of Streptococcus pneumoniae

Masaki Kawabata1, Yuichi Kurono

  • 1Department of Otolaryngology-Head and Neck Surgery, Kagoshima University, Graduate School of Medical and Dental Science, Kagoshima, Japan. supercar@m.kufm.kagoshima-u.ac.jp

The Laryngoscope
|October 14, 2011
PubMed
Abstract

Insights

Viral infections like the common cold can increase the risk of secondary bacterial infections. This study shows that polyinosinic:polycytidylic acid (Poly (I:C)) enhances Streptococcus pneumoniae (Spn) adherence to throat cells by increasing platelet-activating factor receptor (PAF-R) expression.

Area of Science:

  • Microbiology
  • Immunology
  • Cell Biology

Background:

  • Viral upper respiratory tract infections (URIs) frequently precede secondary bacterial infections.
  • The precise mechanisms linking viral URIs to increased bacterial susceptibility require further elucidation.

Purpose of the Study:

  • To investigate the effect of polyinosinic:polycytidylic acid (Poly (I:C)), a viral mimic, on the adherence of Streptococcus pneumoniae (Spn) to human pharyngeal epithelial cells.
  • To determine if Poly (I:C) influences the expression of the platelet-activating factor receptor (PAF-R) in these cells.

Main Methods:

  • Utilized an in vitro model with cultured human pharyngeal epithelial cells (Detroit 562 cell line).
  • Cells were pretreated with Poly (I:C) to induce viral mimicry.
  • Assessed Poly (I:C)-induced PAF-R expression using real-time PCR, flow cytometry, and immunofluorescence microscopy.
  • Quantified Spn adherence to epithelial cells via immunofluorescence microscopy and colony formation assays.

Main Results:

  • Poly (I:C) pretreatment significantly increased both mRNA and protein levels of PAF-R in Detroit 562 cells.
  • Enhanced PAF-R expression correlated with a significant increase in Spn adherence to the pharyngeal epithelial cells.

Conclusions:

  • RNA viral infections, mimicked by Poly (I:C), can upregulate PAF-R expression in epithelial cells.
  • This upregulation of PAF-R may contribute to the increased adherence of Streptococcus pneumoniae, potentially explaining the higher incidence of bacterial infections post-viral URIs.

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