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Related Experiment Videos

Polymorphonuclear leukocyte opsonic receptor expression after hypoxia/reoxygenation

H Simms1, R D'Amico, C Garner

  • 1Brown University School of Medicine, Department of Surgery, Providence, Rhode Island, USA.

The Journal of Laboratory and Clinical Medicine
|April 1, 1996
PubMed
Summary

Hypoxia/reoxygenation primes polymorphonuclear leukocytes (PMNs) for increased receptor expression. This priming enhances PMN function, impacting degranulation and superoxide production through distinct signaling pathways.

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Area of Science:

  • Immunology
  • Cellular Biology
  • Physiology

Background:

  • Hypoxia/reoxygenation (H/R) is a critical condition affecting cellular function.
  • Polymorphonuclear leukocytes (PMNs) play a key role in immune responses.
  • Understanding PMN receptor modulation during H/R is crucial for immune research.

Purpose of the Study:

  • To investigate the effects of H/R on PMN receptor expression (CD32, CD16, CD35, CD11b/CD18).
  • To determine the impact of H/R on PMN degranulation and superoxide anion production.
  • To elucidate the intracellular signaling pathways involved in H/R-induced PMN activation.

Main Methods:

  • PMNs were subjected to hypoxia/reoxygenation (H/R) and stimulated with FMLP or PMA.
  • Flow cytometry was used to assess receptor expression (CD32, CD16, CD35, CD11b/CD18).

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  • Degranulation and superoxide anion production were measured; signaling pathways were investigated using inhibitors.

    • Main Results:

    • H/R primed PMNs for enhanced expression of Fcgamma (CD32, CD16) and complement receptors (CD35, CD11b/CD18) upon stimulation.
    • Maximal receptor upregulation occurred at different time points for FMLP and PMA stimulation.
    • H/R-induced receptor expression involved distinct intracellular pathways, modulated by cytoskeletal elements and protein kinases, and was dependent on NADPH oxidase activity.

    Conclusions:

    • H/R primes PMNs, leading to increased expression of functionally active opsonic receptors.
    • Divergent intracellular signal transduction pathways mediate H/R-induced receptor upregulation.
    • These findings highlight the complex role of H/R in modulating PMN immune function.