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Human neutrophils express the high-affinity receptor for immunoglobulin E (Fc epsilon RI): role in asthma

A S Gounni1, B Lamkhioued, L Koussih

  • 1Meakins Christie Laboratories, McGill University, Montreal, Quebec, Canada. Abdel@meakins.lan.mcgill.ca

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|April 9, 2001
PubMed

Insights

Polymorphonuclear neutrophils (PMNs) express the high-affinity IgE receptor Fc epsilon RI, particularly in asthma. This finding suggests PMNs may contribute to allergic inflammation via IgE-dependent activation.

Area of Science:

  • Immunology
  • Allergy Research
  • Cell Biology

Background:

  • Polymorphonuclear neutrophils (PMNs) are key immune cells involved in host defense and inflammation.
  • IgE receptors, including Fc epsilon RI, are crucial in allergic diseases.
  • Previous studies identified other IgE receptors on PMNs, but Fc epsilon RI expression was unconfirmed.

Purpose of the Study:

  • To investigate the expression and function of the high-affinity IgE receptor, Fc epsilon RI, on PMNs.
  • To determine if Fc epsilon RI on PMNs plays a role in allergic inflammation.

Main Methods:

  • Analysis of Fc epsilon RI alpha chain mRNA and cell surface expression on PMNs from asthmatic subjects.
  • Blocking assays using human IgE Fc fragment and anti-Fc epsilon RI alpha chain antibody (mAb15--1).
  • Immunoreactivity assessment for Fc epsilon RI alpha and beta chains in peripheral blood and bronchoalveolar lavage (BAL) PMNs.

Main Results:

  • Fc epsilon RI alpha chain mRNA and cell surface expression were detected on PMNs from asthmatic individuals.
  • IgE binding to PMNs was primarily mediated by Fc epsilon RI.
  • Intracellular Fc epsilon RI alpha and beta chains were found in asthmatic PMNs.
  • Fc epsilon RI engagement stimulated IL-8 release from PMNs.

Conclusions:

  • PMNs express the Fc epsilon RI receptor.
  • This expression suggests a potential role for PMNs in allergic inflammation through IgE-dependent mechanisms.
  • Further research into PMN activation pathways in allergy is warranted.

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