The role of inflammatory macrophages in pathophysiology of experimental autoimmune myocarditis

Myocarditis is an inflammatory disease of the cardiac muscle characterized by an influx of inflammatory cells, predominantly of myeloid lineage. The progression of myocarditis to a dilated cardiomyopathy phenotype and heart failure is markedly influenced by TGF-ß signalling. The aim of this study was to investigate the role of TGF-ß signalling in inflammatory cardiac macrophages in the development of myocarditis and post-inflammatory fibrosis. Experimental autoimmune myocarditis (EAM) was induced in the LysM-Cre x R26-stop-EYFP x Tgfbr2-fl/fl transgenic mice showing impaired TGF-ß signalling in the myeloid lineage and the LysM-Cre x R26-stop-EYFP control mice. Inflammatory macrophages were sorted from the inflamed hearts and analyzed for differential gene expression using whole genome transcriptomics. Overall design: To investigate the role of TGF-ß signalling in inflammatory cardiac macrophages in the development of myocarditis and post-inflammatory fibrosis we used LysM-Cre x R26-stop-EYFP x Tgfbr2-fl/fl transgenic mice showing impaired TGF-ß signalling in the myeloid lineage and the LysM-Cre x R26-stop-EYFP control mice. We induced myocarditis and collected inflamed heart. Sorted inflammatory cardiac macrophages were used for whole genome transcriptomics.