A role for an animal model in determining the immune mechanisms involved in the pathogenesis of rheumatic heart disease

Abstract

Rheumatic heart disease (RHD) is an autoimmune disease mediated by group A streptococcal (GAS) infection. To study the immune mechanisms underlying RHD, a robust animal model with immunopathology similar to that seen in humans is essential. A Lewis rat model of autoimmune valvulitis has been shown to have potential in investigating the immunopathogenesis of RHD.

In our studies, rats immunized with M protein C-region peptides developed cardiac lesions reflective of those seen in RHD patients, including mononuclear cell infiltration, granuloma formation and valvulitis. Furthermore, mononuclear cells sensitized to cardiac myosin extracted from rat heart lesions were shown to be cross-reactive with streptococcal M protein. These data add further support for using the Lewis rat model for investigating the cell-mediated responses involved in RHD and for testing the safety of GAS peptide-based vaccine candidates.