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Related Experiment Videos

Soluble intercellular adhesion molecule-1 provokes polymorphonuclear leukocyte elastase release by CD18

C C Barnett1, E E Moore, F A Moore

  • 1Department of Surgery, Denver General Hospital, Colo.

Surgery
|August 1, 1996
PubMed
Summary

Soluble intercellular adhesion molecule-1 (sICAM-1) triggers polymorphonuclear leukocyte (PMN) elastase release by interacting with CD18 receptors. This finding suggests a mechanism for how elevated sICAM-1 contributes to organ dysfunction after injury.

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Area of Science:

  • Immunology
  • Cell Biology
  • Pathophysiology

Background:

  • Elevated soluble intercellular adhesion molecule-1 (sICAM-1) levels are linked to multiple organ failure post-injury.
  • sICAM-1 induces secretion in endothelial cells and monocytes during inflammation.
  • sICAM-1 and CD18 receptor cross-linking on polymorphonuclear leukocytes (PMNs) both elicit elastase release.

Purpose of the Study:

  • To investigate if sICAM-1 provokes PMN elastase release via CD18 interaction.
  • To elucidate the role of CD18 in sICAM-1-mediated PMN activation.

Main Methods:

  • sICAM-1 was purified from transfected Chinese hamster ovarian cells.
  • Human PMNs were incubated with sICAM-1 after blockade of CD18 or other beta 2 subunits with monoclonal antibodies.

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  • Elastase activity was quantified using a chromogenic substrate assay.

    • Main Results:

    • Incubation with sICAM-1 significantly increased PMN elastase release (19.2%) compared to controls (2.4%).
    • Blockade of CD18 using specific monoclonal antibodies (TS1/18, 31H8) abrogated sICAM-1-induced elastase release (4.3% and 5.5%).
    • Blockade of CD11a, CD11b, or using nonspecific antibodies did not affect sICAM-1-induced elastase release.

    Conclusions:

    • In vitro studies demonstrate that sICAM-1 provokes PMN elastase release through CD18.
    • This interaction may represent a key mechanism linking elevated circulating sICAM-1 to distal organ dysfunction following injury.