Related Experiment Video
Updated: Apr 12, 2026

An In vitro Model to Study Immune Responses of Human Peripheral Blood Mononuclear Cells to Human Respiratory Syncytial Virus Infection
Published on: December 10, 2013
Treg responses are associated with PM2.5-induced exacerbation of viral myocarditis
Yuquan Xie1, Changyi Gong, Liang Bo
1Department of Cardiology, Xinhua Hospital, Shanghai Jiao Tong University, School of Medicine , Shanghai , China and.
Abstract:
The adverse cardiovascular events induced by ambient fine particles (PM2.5) are paid more attention in the world. The current study was conducted to explore the mechanisms of T regulatory cells (Treg) responses in PM2.5-induced exacerbation of viral myocarditis. The male BALB/c mice were administered an intratracheal (i.t.) instillation of 10 mg/kg b.w. PM2.5 suspension. Twenty-four hours later, the mice were injected intraperitoneally (i.p.) with 100 μl of coxsackievirus B3 (CVB3) diluted in Eagle's minimal essential medium (EMEM). Seven days after the treatment, serum, splenetic, and cardiac tissues were examined. The results showed that pre-exposure to PM2.5 aggravated the cardiac inflammation in the CVB3-infected mice along with an increase of Treg cells in the spleen. The mRNA expressions of interleukin-6 (IL-6), TNF-α, transforming growth factor-β (TGF-β), and Foxp3 were up-regulated in the PM2.5-pretreated mice than that in the CVB3-treated mice. Similar results were found in the sera. In addition, compared with the CVB3-treated mice, the cardiac protein expression of TGF-β increased in the PM2.5-pretreated mice. These results demonstrated that preexposure to PM2.5 exacerbated virus-induced myocarditis possibly through the depression of the immune response and increase of inflammation in myocardium through the Treg responses.
Insights
Fine particles (PM2.5) worsen viral myocarditis by increasing T regulatory cells (Treg) and inflammation. This study reveals PM2.5 exposure exacerbates cardiac damage and immune responses in mice.
Area of Science:
- Environmental Health
- Immunology
- Cardiovascular Research
Background:
- Ambient fine particles (PM2.5) are linked to adverse cardiovascular events.
- Viral myocarditis is a serious cardiac condition.
- The role of T regulatory cells (Treg) in PM2.5-exacerbated viral myocarditis requires further investigation.
Purpose of the Study:
- To explore the mechanisms of T regulatory cell (Treg) responses in PM2.5-induced exacerbation of viral myocarditis.
- To investigate the impact of PM2.5 pre-exposure on cardiac inflammation and immune responses in coxsackievirus B3 (CVB3)-infected mice.
Main Methods:
- Male BALB/c mice were pre-exposed to PM2.5 via intratracheal instillation.
- Mice were subsequently infected with coxsackievirus B3 (CVB3).
- Cardiac tissues, spleen, and serum were analyzed for inflammation markers, Treg cells, and cytokine expression (mRNA and protein).
Main Results:
- PM2.5 pre-exposure aggravated cardiac inflammation in CVB3-infected mice.
- An increase in splenic T regulatory cells (Treg) and elevated mRNA/protein expression of IL-6, TNF-α, TGF-β, and Foxp3 were observed.
- These inflammatory markers were also elevated in serum samples.
Conclusions:
- PM2.5 pre-exposure exacerbates virus-induced myocarditis.
- This exacerbation may occur through the suppression of immune response and increased myocardial inflammation mediated by Treg responses.
More Related Videos
07:35Aggravation of Myocardial Ischemia upon Particulate Matter Exposure in Atherosclerosis Animal Model
Published on: December 10, 2021
10:21Author Spotlight: Exploring the Role of Inflammation in the Co-occurrence of Primary Sjogren's Syndrome and Lung Adenocarcinoma
Published on: September 20, 2024
Related Concept Videos
Myocarditis III: Medical Management
Myocarditis II: Clinical Features and Diagnostic Tests
Myocarditis I: Introduction
Myocarditis IV: Nursing Management
Immune Response Against Viral Pathogens
NK Cells
NK cells are a crucial part of our innate immune system, acting as the first line of defense against viral infections. These cells can recognize and kill infected cells without prior exposure to the virus, effectively slowing down the spread of infection. Additionally, NK cells produce proinflammatory...
Pneumonia II: Pathophysiology