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Human cord blood mononuclear cells decrease cytokines and inflammatory cells in acute myocardial infarction.

Robert J Henning1, Masood Shariff, Ujwala Eadula

  • 1Center for Cardiovascular Research, Department of Medicine of the James A. Haley Medical Center, University of South Florida College of Medicine, Tampa, Florida 33612, USA. Robert.Henning@va.gov

Stem Cells and Development
|April 9, 2008
PubMed
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Human umbilical cord blood mononuclear cells (HUCBC) significantly reduced inflammatory cytokines and cell infiltration in myocardial infarction models. This treatment also limited infarct size and improved left ventricular ejection fraction in rats.

Area of Science:

  • Regenerative Medicine
  • Cardiovascular Research
  • Immunology

Background:

  • Acute myocardial infarction triggers significant cytokine release and inflammatory cell infiltration.
  • Inflammation plays a critical role in infarct expansion and subsequent cardiac dysfunction.
  • Human umbilical cord blood mononuclear cells (HUCBC) possess progenitor cell populations with potential immunomodulatory properties.

Purpose of the Study:

  • To investigate the efficacy of HUCBC in limiting myocardial cytokine expression and inflammatory cell infiltration post-myocardial infarction.
  • To determine if HUCBC treatment can reduce infarct size and improve cardiac function following acute myocardial infarction.

Main Methods:

  • Rats underwent permanent ligation of the left coronary artery to induce myocardial infarction.

Related Experiment Videos

  • Intramyocardial injection of either Isolyte (control) or HUCBC was administered.
  • Myocardial cytokines and inflammatory cell populations (neutrophils, macrophages, lymphocytes) were quantified using antibody arrays and flow cytometry at various time points.
  • Left ventricular infarct size and ejection fraction were assessed at 72 hours and 2 months post-infarction, respectively.

    • Main Results:

    • Isolyte-treated hearts showed significant increases in pro-inflammatory cytokines (TNF-α, MCP-1, IL-1β, etc.) and inflammatory cell infiltration compared to controls.
    • HUCBC treatment significantly attenuated the expression of these cytokines and reduced neutrophil, macrophage, and lymphocyte infiltration.
    • Left ventricular infarct size was significantly smaller in HUCBC-treated hearts (6.9% vs. 15.7%).
    • Left ventricular ejection fraction was significantly improved in HUCBC-treated rats at 1 and 2 months post-infarction.

    Conclusions:

    • HUCBC administration effectively limits the acute inflammatory response in myocardial infarction.
    • HUCBC treatment reduces infarct size and preserves left ventricular function.
    • The immunomodulatory effects of HUCBC are a key mechanism for limiting myocardial damage and improving cardiac outcomes.