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Related Experiment Videos

Interactions between endothelial cells and effector cells in allergic inflammation

A B Tonnel1, P Gosset, S Molet

  • 1Unité INSERM n degree 416, Institut Pasteur Lille, France.

Annals of the New York Academy of Sciences
|October 31, 1996
PubMed
Summary

Endothelial cells (EC) play a key role in lung inflammation by interacting with inflammatory cells. Histamine and eosinophils significantly influence EC responses, impacting adhesion molecule expression and cytokine production in allergic reactions.

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Area of Science:

  • Immunology
  • Cell Biology
  • Pulmonology

Background:

  • Local inflammatory responses in the lungs involve complex interactions between inflammatory and resident structural cells.
  • Endothelial cells (EC) are critical structural cells that regulate leukocyte traffic and amplify leukocyte activation via cytokine and chemokine production.

Purpose of the Study:

  • To investigate the role of endothelial cells (EC) in the inflammatory response within the lung.
  • To examine how inflammatory cells like macrophages, mast cells, and eosinophils influence EC behavior.

Main Methods:

  • Cultured human umbilical vein endothelial cells (HUVEC) were exposed to supernatants from alveolar macrophages of asthmatic patients.
  • HUVEC were treated with histamine, a mast cell mediator, and histamine receptor antagonists.

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  • HUVEC were exposed to purified eosinophils from patients with hypereosinophilia.
  • Main Results:

    • Macrophage supernatants induced TNF alpha-dependent overexpression of ICAM-1 and E-selectin on HUVEC.
    • Histamine induced concentration-dependent IL-6 and IL-8 secretion by HUVEC, inhibited by H1/H2 receptor antagonists.
    • Eosinophils increased adhesion molecule expression and chemokine production by HUVEC, with specific mediators under investigation.

    Conclusions:

    • Endothelial cells are key players in the local inflammatory response in the lung, responding to mediators from macrophages, mast cells, and eosinophils.
    • Allergen-induced inflammatory cells modulate endothelial cell function, contributing to the late-phase asthmatic reaction.
    • Further research is needed to identify specific eosinophil products involved in endothelial cell activation.