Neutrophil Mac-1 and MEL-14 adhesion proteins inversely regulated by chemotactic factors

T K Kishimoto1, M A Jutila, E L Berg

  • 1Department of Pathology, Stanford University, CA 94305.

Science (New York, N.Y.)
|September 15, 1989
PubMed

Insights

Neutrophil Mac-1 increases with activation, while gp100MEL-14 sheds rapidly. This shedding may prevent activated neutrophils from damaging healthy tissues during inflammation.

Area of Science:

  • Immunology
  • Cell Biology
  • Inflammation Research

Background:

  • Neutrophil extravasation is crucial during inflammation, involving adhesion proteins like Mac-1 and gp100MEL-14.
  • Mac-1 expression and activity significantly increase upon neutrophil activation.
  • gp100MEL-14 is rapidly shed from the neutrophil surface after activation.

Purpose of the Study:

  • To investigate the role of gp100MEL-14 shedding in neutrophil function during inflammation.
  • To understand the differential regulation of Mac-1 and gp100MEL-14 during neutrophil activation and extravasation.

Main Methods:

  • Neutrophil activation assays using chemotactic factors and phorbol esters.
  • Measurement of Mac-1 and gp100MEL-14 expression and shedding.
  • Immunohistochemical analysis of gp100MEL-14 on extravasated neutrophils in inflamed tissue.

Main Results:

  • Neutrophil activation led to a rapid shedding of gp100MEL-14, releasing a 96-kDa fragment.
  • gp100MEL-14 was downregulated on neutrophils that had extravasated into inflamed tissue.
  • Mac-1 expression and activity were upregulated following neutrophil activation.

Conclusions:

  • Rapid shedding of gp100MEL-14 upon activation is a key regulatory mechanism.
  • This shedding may prevent activated neutrophils from binding to and damaging healthy endothelium.
  • gp100MEL-14 might play a role in the initial adhesion of unactivated neutrophils to the endothelium.

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