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Neutrophil and Macrophage Cell Surface Colony-Stimulating Factor 1 Shed by ADAM17 Drives Mouse Macrophage

Jingjing Tang1, Jeremy M Frey2, Carole L Wilson2

  • 1Department of Pathology, University of Washington, Seattle, Washington, USA jjtang@uw.edu bornf@uw.edu.

Molecular and Cellular Biology
|June 13, 2018
PubMed

Insights

The leukocyte protease ADAM17 is crucial for macrophage proliferation during inflammation by shedding cell surface CSF-1. Its absence impairs this process, highlighting a new therapeutic target for inflammatory diseases.

Area of Science:

  • Immunology
  • Cell Biology
  • Inflammation Research

Background:

  • Macrophages play key roles in acute and chronic inflammatory diseases.
  • Macrophage proliferation following monocyte recruitment is increasingly recognized in inflammation.

Purpose of the Study:

  • To investigate the role of the leukocyte protease ADAM17 in macrophage proliferation during inflammation.
  • To elucidate the mechanism by which ADAM17 influences macrophage proliferation.

Main Methods:

  • Utilized an acute peritonitis mouse model to study macrophage proliferation.
  • Assessed macrophage colony-stimulating factor 1 (CSF-1) levels and ADAM17 activity.
  • Investigated the role of iRhom2 in ADAM17 function and CSF-1 shedding.

Main Results:

  • Mice lacking ADAM17 exhibited a significant defect in macrophage proliferation.
  • This defect was linked to reduced peritoneal CSF-1, which was rescued by CSF-1 administration.
  • ADAM17 cleaves cell surface CSF-1 (csCSF-1), with neutrophils and macrophages as major sources.
  • iRhom2 regulates ADAM17-mediated csCSF-1 shedding from neutrophils and macrophages, impacting proliferation.
  • ADAM17-mediated macrophage proliferation is transient in acute inflammation but prolonged in chronic conditions like atherosclerosis.

Conclusions:

  • ADAM17 promotes macrophage proliferation in both acute and chronic inflammatory settings.
  • The study reveals a novel mechanism involving ADAM17-mediated csCSF-1 shedding that regulates macrophage expansion.
  • This pathway represents a potential therapeutic target for modulating inflammatory responses.
Keywords:
ADAM17CSF-1cell proliferationiRhom2inflammationmacrophages

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