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Macrophage migration inhibitory factor delays apoptosis in neutrophils by inhibiting the mitochondria-dependent death

Ralf Baumann1, Carmen Casaulta, Dagmar Simon

  • 1Department of Pharmacology, University of Bern, Switzerland.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|December 6, 2003
PubMed

Insights

Macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine that prevents neutrophil death. This finding suggests MIF plays a role in infectious diseases by prolonging neutrophil survival.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Medicine

Background:

  • Macrophage migration inhibitory factor (MIF) is a known pro-inflammatory cytokine.
  • MIF activates macrophages and T cells.
  • Neutrophil apoptosis is crucial for resolving inflammation and preventing tissue damage.

Purpose of the Study:

  • To investigate the effect of MIF on neutrophil apoptosis.
  • To elucidate the molecular mechanisms by which MIF influences neutrophil survival.
  • To explore the potential role of MIF in cystic fibrosis.

Main Methods:

  • Recombinant MIF was used to treat human neutrophils in vitro.
  • Western blotting was employed to assess the cleavage of Bcl-2 family proteins (Bid, Bax).
  • Mitochondrial assays measured the release of cytochrome c and Smac.
  • Caspase-3 activity was quantified.
  • MIF plasma levels were measured in patients with cystic fibrosis.

Main Results:

  • Recombinant MIF significantly delayed neutrophil apoptosis in a dose- and time-dependent manner.
  • MIF inhibited the cleavage of proapoptotic proteins Bid and Bax.
  • MIF prevented the release of cytochrome c and Smac from mitochondria.
  • MIF suppressed caspase-3 activation.
  • Elevated MIF plasma levels were observed in cystic fibrosis patients.

Conclusions:

  • MIF acts as a survival factor for human neutrophils.
  • MIF inhibits apoptosis through pathways involving mitochondria and caspase activation.
  • Increased MIF levels in cystic fibrosis suggest a role in delayed neutrophil apoptosis in this disease.
  • These findings have potential implications for managing infectious diseases.

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