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Related Experiment Videos

Chronic heart failure and the immune system.

Daniela Mari1, Federica Di Berardino, Massimo Cugno

  • 1Department of Internal Medicine, University of Milan, Maggiore Hospital IRCCS, Via Pace 15, 20122 Milan, Italy. daniela.mari@unimi.it

Clinical Reviews in Allergy & Immunology
|October 31, 2002
PubMed
Summary

Immune system activation, involving cytokines and chemokines, plays a key role in chronic heart failure (CHF) progression. Research explores gut or heart origins of this inflammation, suggesting new anti-cytokine therapies for CHF.

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Area of Science:

  • Cardiology
  • Immunology
  • Pathophysiology

Background:

  • Chronic heart failure (CHF) pathogenesis involves immune mechanisms.
  • Proinflammatory cytokines, chemokines, adhesion molecules, autoantibodies, nitric oxide (NO), and endothelin-1 are implicated in CHF progression.
  • The precise origin of immune activation in CHF remains unclear.

Purpose of the Study:

  • To investigate the role of immune mechanisms in chronic heart failure (CHF).
  • To explore potential sources of immune activation in CHF.
  • To identify new therapeutic strategies for CHF based on immune system modulation.

Main Methods:

  • Review of existing experimental and clinical data on immune involvement in CHF.
  • Analysis of proposed hypotheses regarding the origin of immune activation (gut vs. heart).

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  • Consideration of systemic hypoxia as a contributing factor to immune activation.

    • Main Results:

    • Evidence supports immune system involvement in CHF, including cytokines (interleukin-1, -2, -6, tumor necrosis factor) and chemokines.
    • Two main hypotheses for immune activation: bacterial translocation from bowel edema or cytokine production by the failing heart.
    • Systemic hypoxia is identified as a potent stimulus for immune activation and cytokine production in CHF.

    Conclusions:

    • The immune system, particularly cytokines, is crucial in CHF pathogenesis.
    • Neither gut nor heart alone fully explains the systemic inflammation in CHF; a multifactorial origin is likely.
    • Targeting immune pathways, such as with anti-cytokine drugs, offers promising therapeutic avenues for CHF.