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Double-stranded RNA induces S100 gene expression by a cycloheximide-sensitive factor

Andreas Voss1, Kirsten Gescher, Andreas Hensel

  • 1Institute of Immunology, University of Witten-Herdecke, Germany.

FEBS Letters
|January 3, 2012
PubMed

Insights

Polyriboinosinic:polyribouridylic acid (polyI:C) triggers inflammation by upregulating damage-associated molecular pattern (DAMP) molecules S100A8 and S100A9. These S100A8/A9 molecules play a role in antiviral defense, independent of interferon signaling.

Area of Science:

  • Immunology
  • Molecular Biology
  • Virology

Background:

  • Viral double-stranded RNA (dsRNA) and its analog polyI:C activate inflammatory pathways.
  • The precise molecular mechanisms linking dsRNA recognition to specific gene expression, particularly inflammatory mediators, require further elucidation.

Purpose of the Study:

  • To investigate the specific gene expression patterns induced by polyI:C, focusing on damage-associated molecular pattern (DAMP) molecules.
  • To determine the role of cytokines and interferons in the polyI:C-mediated induction of S100A8 and S100A9.

Main Methods:

  • Treatment of cells with polyI:C.
  • Analysis of gene expression using cycloheximide and Brefeldin A to distinguish primary and secondary response genes.
  • Quantification of various interferon and cytokine gene expression levels.

Main Results:

  • PolyI:C specifically induced the expression of S100A8 and S100A9, while other S100 genes remained unaffected.
  • S100A8 and S100A9 were identified as secondary response genes, dependent on polyI:C-induced cytokines.
  • Type I and III interferons (IFNβ, IL-20, IL-24, IFNλ/IL-29) were expressed but did not directly induce S100A8/S100A9.

Conclusions:

  • S100A8 and S100A9 are key players in the inflammatory response to viral dsRNA analogs.
  • The induction of S100A8/S100A9 involves a cytokine-dependent secondary response pathway.
  • These findings suggest a role for S100A8/S100A9 in antiviral defense mechanisms.

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