Key Points
- To determine the role and regulation of intercellular adhesion molecule-1 (ICAM-1) in cell-mediated myocardial damage during acute coxsackievirus B3 infection.
- Assessed ICAM-1 expression via immunofluorescence in murine heart tissue following coxsackievirus B3 (CVB3) infection.
- Evaluated ICAM-1 induction in cultured cardiac myocytes treated with IFN-gamma and TNF-alpha using immunofluorescence and Northern blot hybridization.
- Administered F(ab')2 fragments of an anti-ICAM-1 monoclonal antibody in vivo to measure changes in CVB3-induced myocardial inflammation.
- CVB3-induced acute myocarditis caused marked upregulation of ICAM-1 expression in myocardial cells.
- Proinflammatory cytokines IFN-gamma and TNF-alpha synthesized by infiltrating immune cells induced ICAM-1 expression in cultured cardiac myocytes in vitro.
- In vivo blockade with anti-ICAM-1 mAb F(ab')2 fragments significantly reduced myocardial inflammation in mice infected with CVB3.
Structured PICO
Does in vivo administration of anti-ICAM-1 mAbs reduce myocardial inflammation in a murine model of acute viral myocarditis?
PPopulationMurine model of acute myocarditis caused by coxsackievirus B3 (CVB3) and cultured cardiac myocytes
IInterventionIn vivo administration of F(ab')2 fragments of an anti-ICAM-1 monoclonal antibody
OOutcomeMyocardial inflammation and expression of ICAM-1surrogate
The expression of ICAM-1 in myocardial cells plays a critical role in cell-mediated cytotoxicity in acute viral myocarditis, and its blockade reduces myocardial inflammation in a murine model.