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Related Experiment Videos

Captopril prevents experimental autoimmune myocarditis.

Lisa M Godsel1, Juan S Leon, Kegiang Wang

  • 1Department of Microbiology-Immunology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|June 21, 2003
PubMed
Summary

Captopril, an angiotensin-converting enzyme inhibitor, significantly reduces experimental autoimmune myocarditis severity in mice. This treatment impacts cell-mediated immunity without affecting antibody production.

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Area of Science:

  • Immunology
  • Cardiology
  • Pharmacology

Background:

  • Autoimmune myocarditis is a severe cardiac condition.
  • Captopril is an angiotensin-converting enzyme inhibitor used for cardiomyopathies.
  • The effect of captopril on autoimmune myocarditis is not well-established.

Purpose of the Study:

  • To investigate the therapeutic effect of captopril on myosin-induced experimental autoimmune myocarditis.
  • To elucidate the immunological mechanisms underlying captopril's action in this model.

Main Methods:

  • Experimental autoimmune myocarditis was induced in A/J mice using cardiac myosin immunization.
  • Mice received captopril in drinking water or direct injection at the test site.
  • Cell-mediated immunity (delayed-type hypersensitivity) and antibody production were assessed.

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  • T cell proliferation and cytokine secretion (IFN-gamma, IL-2) were evaluated in vitro and in vivo.

    • Main Results:

    • Captopril significantly reduced the incidence and severity of autoimmune myocarditis.
    • Reduced heart weight to body weight ratio and heart weight were observed in captopril-treated mice.
    • Captopril suppressed myosin-specific delayed-type hypersensitivity (DTH) but not anti-myosin antibody production.
    • Captopril did not directly impair antigen-specific T cell proliferation or cytokine secretion.

    Conclusions:

    • Captopril ameliorates experimental autoimmune myocarditis.
    • The therapeutic effect may involve interference with inflammatory cell recruitment and the local inflammatory environment.
    • Captopril's action appears to be independent of direct effects on antigen-specific T cell responsiveness.