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Related Experiment Videos

Acetaminophen inhibits the human polymorphonuclear leukocyte function in vitro.

E A Shalabi1

  • 1Department of Physiology, College of Medicine, King Saud University, Riyadh, Saudi Arabia.

Immunopharmacology
|July 1, 1992
PubMed
Summary

Acetaminophen (Am) significantly inhibits human polymorphonuclear leukocytes (PMNs) oxidative burst and function in vitro. This effect was observed on PMN chemiluminescence, superoxide generation, and phagocytic activity.

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Area of Science:

  • Immunology
  • Pharmacology
  • Cell Biology

Background:

  • Polymorphonuclear leukocytes (PMNs) are crucial immune cells involved in the oxidative respiratory burst.
  • Acetaminophen (Am) is a widely used analgesic and antipyretic agent.
  • The impact of Acetaminophen on PMN function requires further investigation.

Purpose of the Study:

  • To investigate the effect of Acetaminophen (Am) on the oxidative respiratory burst of isolated human polymorphonuclear leukocytes (PMNs).
  • To assess the impact of Am on PMN-mediated chemiluminescence, superoxide generation, and phagocytosis.

Main Methods:

  • Isolated human PMNs were stimulated with phorbol myristate acetate (PMA) or opsonized zymosan.
  • Luminol-chemiluminescence (CL) was measured to assess oxidative burst.

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  • Superoxide (O2-) generation was quantified using ferricytochrome c reduction.
  • Phagocytic activity was evaluated by the ingestion of opsonized dead yeast.

    • Main Results:

    • Acetaminophen (Am) demonstrated a concentration-dependent inhibition of PMN luminol-chemiluminescence (CL) response.
    • Am significantly reduced superoxide generation and phagocytic activity in stimulated PMNs.
    • The inhibitory effect of Am on CL was partially reversible and enhanced by hydroxyl radical scavengers.

    Conclusions:

    • Acetaminophen (Am) significantly inhibits key functions of human polymorphonuclear leukocytes (PMNs) in vitro.
    • These findings suggest that Am can modulate innate immune cell responses, impacting oxidative burst and phagocytosis.