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Modulation of the inflammatory response by products released from human polymorphonuclear leukocytes during

D G Wright1, J I Gallin

  • 1Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases National Institutes of Health, Bethesda, Maryland.

Inflammation
|November 7, 2013
PubMed

Insights

Human polymorphonuclear leukocytes (PMNs) release a product during phagocytosis that activates complement, generating C5a and enhancing chemotaxis. PMNs also release a C5a inactivator, modulating inflammatory responses.

Area of Science:

  • Immunology
  • Cell Biology
  • Inflammation Research

Background:

  • Polymorphonuclear leukocytes (PMNs) are key immune cells involved in phagocytosis.
  • Chemotaxis is crucial for immune cell migration to sites of inflammation.
  • The complement system plays a vital role in innate immunity and inflammation.

Purpose of the Study:

  • To investigate the nature of the product released by PMNs during phagocytosis that affects human serum.
  • To determine the role of this PMN-derived product in generating chemotactic activity.
  • To elucidate the mechanisms of complement activation and C5a generation by PMNs.

Main Methods:

  • Phagocytosis of latex particles by human PMNs.
  • Gel-filtration chromatography to analyze serum components.
  • Complement activation studies using C5, EDTA, magnesium-EGTA, and deficient/heated sera.

Main Results:

  • PMNs release a serum activator during phagocytosis, with maximal release at 20-30 minutes.
  • This activator generates significant chemotactic activity, primarily due to C5a.
  • C5a generation involves both direct C5 cleavage and complement system activation via classical and alternate pathways.
  • PMNs also release a C5a chemotactic activity inactivator.

Conclusions:

  • Phagocytizing PMNs possess secretory functions that modulate complement system activation.
  • PMN-derived factors contribute to the generation and regulation of inflammatory responses.
  • These findings highlight the complex role of PMNs in orchestrating localized inflammation.

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