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TRAF6: A player in CVB3-induced myocarditis?

Oana N Ursu1, Tina Beyer1, Martina Sauter2

  • 1University Hospital Tübingen Medical Clinic, Department of Sports Medicine, Hoppe-Seyler-Str. 6, D-72076 Tübingen, Germany; University Hospital Tübingen, Department of Molecular Pathology, Institute for Pathology and Neuropathology, Liebermeisterstr. 8, D-72076 Tübingen, Germany.

Cytokine
|September 10, 2017
PubMed

Insights

Coxsackievirus B3 (CVB3) infection increases TNF receptor-associated factor 6 (TRAF6) levels in heart tissue and cells. However, TRAF6 induction is not essential for CVB3-induced nuclear factor kappa B (NFκB) activation.

Area of Science:

  • Virology
  • Immunology
  • Cardiology

Background:

  • Coxsackievirus B3 (CVB3) is a primary cause of myocarditis, potentially leading to dilated cardiomyopathy and heart failure.
  • The precise mechanisms underlying CVB3-induced heart disease chronification remain unclear.
  • TNF receptor-associated factor 6 (TRAF6) is a key signal transduction protein involved in immune responses downstream of cytokine receptors.

Purpose of the Study:

  • To investigate the role of TRAF6 gene expression in CVB3 infection.
  • To determine the relationship between TRAF6 levels and nuclear factor kappa B (NFκB) activation during CVB3 infection.
  • To analyze TRAF6's functional significance in CVB3-induced pathogenesis.

Main Methods:

  • Analysis of TRAF6 gene expression in heart tissue from susceptible and non-susceptible mouse strains post-CVB3 infection.
  • Assessment of TRAF6 levels and NFκB activity in CVB3-infected HeLa cells.
  • Functional analysis of TRAF6 using siRNA-mediated knockdown in HeLa cells.

Main Results:

  • TRAF6 expression was upregulated in CVB3-infected heart tissues of different mouse strains, with varying degrees of induction.
  • CVB3 infection moderately increased TRAF6 levels and strongly enhanced NFκB activity in HeLa cells.
  • Reduction of TRAF6 expression did not impact NFκB activation in response to CVB3 infection.

Conclusions:

  • CVB3 infection leads to increased TRAF6 expression in cardiac tissue and cells.
  • TRAF6 induction appears to be a consequence of CVB3 infection, but not a prerequisite for NFκB activation.
  • These findings suggest TRAF6 is not essential for the early NFκB-mediated response to CVB3 infection.

Keywords:
CVB3HeLa cellsMyocarditisNFkappaBTRAF6

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