Mononuclear cell secretome protects from experimental autoimmune myocarditis

Eur Heart J. 2015 Mar 14;36(11):676-85. doi: 10.1093/eurheartj/ehs459. Epub 2013 Jan 14.

Abstract

Aims: Supernatants of serum-free cultured mononuclear cells (MNC) contain a mix of immunomodulating factors (secretome), which have been shown to attenuate detrimental inflammatory responses following myocardial ischaemia. Inflammatory dilated cardiomyopathy (iDCM) is a common cause of heart failure in young patients. Experimental autoimmune myocarditis (EAM) is a CD4+ T cell-dependent model, which mirrors important pathogenic aspects of iDCM. The aim of this study was to determine the influence of MNC secretome on myocardial inflammation in the EAM model.

Methods and results: BALB/c mice were immunized twice with an alpha myosin heavy chain peptide together with Complete Freund adjuvant. Supernatants from mouse mononuclear cells were collected, dialysed, and injected i.p. at Day 0, Day 7, or Day 14, respectively. Myocarditis severity, T cell responses, and autoantibody formation were assessed at Day 21. The impact of MNC secretome on CD4+ T cell function and viability was evaluated using in vitro proliferation and cell viability assays. A single high-dose application of MNC secretome, injected at Day 14 after the first immunization, effectively attenuated myocardial inflammation. Mechanistically, MNC secretome induced caspase-8-dependent apoptosis in autoreactive CD4+ T cells.

Conclusion: MNC secretome abrogated myocardial inflammation in a CD4+ T cell-dependent animal model of autoimmune myocarditis. This anti-inflammatory effect of MNC secretome suggests a novel and simple potential treatment concept for inflammatory heart diseases.

Keywords: Conditioned medium; Mononuclear cells; Myocarditis; Secretome.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies / pharmacology
  • Apoptosis / physiology
  • Autoantibodies / metabolism
  • Autoimmune Diseases / prevention & control*
  • CD4-CD8 Ratio
  • CD4-Positive T-Lymphocytes / physiology*
  • CD40 Ligand / immunology
  • CD8-Positive T-Lymphocytes / physiology
  • Caspase Inhibitors / pharmacology
  • Cell Proliferation / physiology
  • Cells, Cultured
  • Cytokines / metabolism
  • Dendritic Cells / physiology
  • Disease Models, Animal
  • Fas Ligand Protein / immunology
  • Humans
  • Mice, Inbred BALB C
  • Myocarditis / prevention & control*
  • Myosin Heavy Chains / pharmacology*
  • Receptors, TNF-Related Apoptosis-Inducing Ligand / immunology
  • Spleen / cytology

Substances

  • Antibodies
  • Autoantibodies
  • Caspase Inhibitors
  • Cytokines
  • Fas Ligand Protein
  • Fasl protein, mouse
  • Myh6 protein, mouse
  • Receptors, TNF-Related Apoptosis-Inducing Ligand
  • CD40 Ligand
  • Myosin Heavy Chains