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Matrix metalloproteinase-9 release from human leukocytes

Shigeru Takafuji1, Akira Ishida, Yuji Miyakuni

  • 1Department of Internal Medicine, Toyoko Hospital, St. Marianna University School of Medicine, 3-435 Kosugi, Nakahara-ku, Kawasaki-City, Kanagawa 211-0063, Japan. takafuji@marianna-u.ac.jp

Journal of Investigational Allergology & Clinical Immunology
|July 17, 2003
PubMed

Insights

Neutrophils release matrix metalloproteinase-9 (MMP-9) in response to specific stimuli like FMLP. This release, enhanced by GM-CSF and mediated by G-proteins, may contribute to inflammatory lung diseases.

Area of Science:

  • Immunology
  • Respiratory Medicine
  • Cell Biology

Background:

  • Proteinases are implicated in the pathogenesis of bronchial asthma and COPD.
  • The precise mechanisms of proteinase release from inflammatory cells remain unclear.

Purpose of the Study:

  • To investigate the release of matrix metalloproteinase-9 (MMP-9) from human leukocytes.
  • To identify the primary cell type responsible for MMP-9 release and the stimuli that trigger it.

Main Methods:

  • Human leukocytes (mononuclear cells, neutrophils, eosinophils) were isolated.
  • Cells were incubated with soluble agonists: C5a, FMLP, and PAF.
  • MMP-9 levels in supernatants were quantified using ELISA.
  • The role of GM-CSF and pertussis toxin (PTX)-sensitive G-proteins was assessed.

Main Results:

  • Neutrophils were the primary source of MMP-9 release among tested leukocytes.
  • FMLP was the most potent stimulus for MMP-9 release from neutrophils.
  • Granulocyte-macrophage colony-stimulating factor (GM-CSF) significantly enhanced FMLP-induced MMP-9 release.
  • Pertussis toxin (PTX) inhibited FMLP-induced MMP-9 release, indicating G-protein involvement.

Conclusions:

  • Neutrophils release substantial amounts of MMP-9, particularly in response to FMLP.
  • The signaling pathway for FMLP-induced MMP-9 release involves PTX-sensitive G-proteins.
  • Neutrophil-derived MMP-9 may play a role in the pathogenesis of bronchial asthma and COPD.

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