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Progranulin ameliorates coxsackievirus-B3-induced viral myocarditis by downregulating Th1 and Th17 cells

Li Li1, Ling Li1, Lili Xiao1

  • 1Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, No. 1, Jianshe Dong Road, Zhengzhou, Henan 450052, China.

Experimental Cell Research
|April 7, 2018
PubMed

Insights

Progranulin (PGRN) levels increase during Coxsackievirus B3 (CVB3) infection, reducing viral myocarditis severity. PGRN deficiency worsens disease, while PGRN treatment offers therapeutic potential for this cardiac condition.

Area of Science:

  • Cardiology
  • Immunology
  • Virology

Background:

  • Viral myocarditis, often caused by Coxsackievirus B3 (CVB3), is a significant cause of sudden cardiac death in young adults.
  • Progranulin (PGRN), a growth factor with known anti-inflammatory properties, has an uncharacterized role in viral myocarditis pathogenesis.

Purpose of the Study:

  • To investigate the expression and function of Progranulin (PGRN) in the context of Coxsackievirus B3 (CVB3)-induced viral myocarditis.

Main Methods:

  • Assessed PGRN levels in plasma and cardiac tissues of infected mice.
  • Utilized PGRN-deficient mice and recombinant PGRN treatment to evaluate its effects on CVB3-induced myocarditis.
  • Analyzed immune cell responses (Th1, Th17, Treg) and cytokine production in vitro and in vivo.
  • Investigated the role of the JAK/STAT pathway in PGRN-mediated immune regulation.

Main Results:

  • PGRN levels were significantly upregulated post-CVB3 infection and negatively correlated with disease severity.
  • PGRN deficiency exacerbated viral myocarditis, while PGRN treatment attenuated the condition in mice.
  • PGRN suppressed Th1 and Th17 cell responses and cytokine production, independent of Treg cells.
  • PGRN regulated Th1 and Th17 cell differentiation by inhibiting the JAK/STAT pathway.

Conclusions:

  • Progranulin (PGRN) plays a critical protective role in mitigating Coxsackievirus B3 (CVB3)-induced viral myocarditis.
  • PGRN demonstrates potential as a novel therapeutic target for treating viral myocarditis.

Keywords:
Coxsackievirus B3PGRNTh1 cellsTh17 cellsViral myocarditis

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