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Expression of vascular cell adhesion molecule-1 in murine hearts with acute myocarditis caused by coxsackievirus B3
1Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
Abstract:
Cell-mediated autoimmunity has been strongly implicated in the pathogenesis of the myocardial cell damage involved in viral myocarditis. Using a murine model of acute myocarditis caused by Coxsackievirus B3 (CVB3), perforin-expressing killer cells have been shown to infiltrate the heart, and intercellular adhesion molecular-1 (ICAM-1) together with major histocompatibility complex (MHC) antigen was induced on myocardial cells in acute viral myocarditis. To clarify the immunological mechanisms in more detail, the expression of vascular cell adhesion molecular-1 (VCAM-1) has been examined in the heart of acute myocarditis and on cultured cardiac myocytes treated with interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF-alpha). The effects of in vivo antibody treatment to VCAM-1 on myocardial damage involved in acute myocarditis were also analysed. CVB3-induced myocarditis resulted in enhanced expression of VCAM-1 on myocardial cells. VCAM-1 expression was also induced on cultured cardiac myocytes by treatment with IFN-gamma and TNF-alpha. The in vivo antibody treatment to VCAM-1 decreased the myocardial damage to some extent, but the effects were not statistically significant. These data suggest that the expression of VCAM-1 on myocardial cells may play at least a partial role in the myocardial damage involved in acute viral myocarditis.
Insights
Vascular cell adhesion molecule-1 (VCAM-1) is expressed on heart cells during viral myocarditis. Targeting VCAM-1 showed a trend toward reducing heart damage, suggesting a partial role in viral myocarditis pathogenesis.
Area of Science:
- Immunology
- Cardiovascular Research
- Pathogenesis of Viral Infections
Background:
- Cell-mediated autoimmunity is implicated in viral myocarditis.
- Coxsackievirus B3 (CVB3) infection in mice shows killer cell infiltration and induced intercellular adhesion molecule-1 (ICAM-1) and major histocompatibility complex (MHC) on myocardial cells.
Purpose of the Study:
- To investigate the role of vascular cell adhesion molecule-1 (VCAM-1) in myocardial damage during acute viral myocarditis.
- To examine VCAM-1 expression on cardiac myocytes treated with interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α).
- To assess the impact of in vivo VCAM-1 blockade on myocarditis-induced cardiac damage.
Main Methods:
- Examined VCAM-1 expression in the hearts of mice with CVB3-induced myocarditis.
- Induced VCAM-1 expression on cultured cardiac myocytes using IFN-γ and TNF-α.
- Administered in vivo antibody treatment targeting VCAM-1 in the murine myocarditis model.
Main Results:
- CVB3 infection led to increased VCAM-1 expression on myocardial cells.
- IFN-γ and TNF-α treatment induced VCAM-1 expression on cultured cardiac myocytes.
- In vivo VCAM-1 blockade partially reduced myocardial damage, though not to a statistically significant extent.
Conclusions:
- VCAM-1 is expressed on myocardial cells during viral myocarditis.
- VCAM-1 may contribute partially to the pathogenesis of myocardial damage in acute viral myocarditis.