Preexposure to PM2.5 exacerbates acute viral myocarditis associated with Th17 cell

Yuquan Xie1, Xian Zhang, Zhenyong Tian

  • 1Department of Cardiology, Xinhua Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, 200092 China.

Abstract

Insights

Fine particle (PM2.5) exposure worsened viral myocarditis by increasing Th17 cell activity and viral replication. This suggests air pollution contributes to cardiovascular disease development.

Area of Science:

  • Environmental Health
  • Immunology
  • Cardiovascular Research

Background:

  • Ambient fine particles (PM2.5) are recognized risk factors for cardiovascular events.
  • The role of PM2.5 in viral myocarditis pathogenesis requires further elucidation.
  • T helper 17 (Th17) cells are implicated in inflammatory and immune responses.

Purpose of the Study:

  • To investigate the association between PM2.5 exposure and viral myocarditis.
  • To explore the functional mechanism of Th17 cells in PM2.5-exacerbated viral myocarditis.
  • To understand the impact of PM2.5 on viral replication and cardiac/pulmonary injury.

Main Methods:

  • Male BALB/c mice were intratracheally instilled with PM2.5.
  • Mice were subsequently infected with coxsackievirus B3 (CVB3).
  • Cardiac and pulmonary tissues were analyzed for injury, viral load, and immune cell markers.

Main Results:

  • PM2.5 pre-exposure increased cardiac and pulmonary injury and viral replication in CVB3-infected mice.
  • Increased CD4(+) IL-17(+) cells, IL-17A, perforin, TGF-β, and RORγt were observed.
  • Cardiac IL-17A and MMP-2 increased, while IFN-γ and TIMP-1 decreased post-PM2.5 exposure.

Conclusions:

  • PM2.5 exposure exacerbates virus-induced myocarditis via Th17-mediated mechanisms.
  • Increased viral replication, perforin response, and MMP-2/TIMP-1 imbalance contribute to disease severity.
  • Findings support epidemiological data linking ambient particles to cardiovascular disease incidence.

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