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Pathogenic bacteria and TNF do not induce production of macrophage migration inhibitory factor (MIF) by human

Suzanna E L Temple1, Karey Y Cheong, Patricia Price

  • 1School of Medicine and Pharmacology, RPH Unit (M570), University of Western Australia, 35 Stirling Highway, Crawley, WA 6009, Australia. stemple@meddent.uwa.edu.au

Cytokine
|May 2, 2009
PubMed

Insights

Elevated serum macrophage migration inhibitory factor (MIF) in sepsis may not stem from direct bacterial stimulation of blood leukocytes. This study found bacteria and TNF did not increase MIF production by leukocytes, suggesting other sources for elevated MIF levels.

Area of Science:

  • Immunology
  • Sepsis Pathophysiology

Background:

  • Elevated serum macrophage migration inhibitory factor (MIF) correlates with severe sepsis.
  • The source of increased MIF during sepsis remains unclear.

Purpose of the Study:

  • To investigate whether bacteria or TNF directly stimulate MIF production in human blood leukocytes.
  • To identify the primary leukocyte subset responsible for MIF synthesis.

Main Methods:

  • Exposure of human blood leukocytes (n=28) to Escherichia coli and Streptococcus pneumoniae.
  • Measurement of MIF mRNA and protein levels.
  • Analysis of MIF production by CD14(+) monocytes.
  • Assessment of MIF induction by Tumor Necrosis Factor (TNF).

Main Results:

  • Bacteria did not significantly increase MIF mRNA or secreted protein levels in leukocytes.
  • CD14(+) monocytes were the main source of MIF, both before and after stimulation.
  • TNF exposure did not induce MIF production by leukocytes.

Conclusions:

  • Elevated serum MIF in sepsis may not originate from direct bacterial or TNF-induced stimulation of blood leukocytes.
  • Further research is needed to identify the source of serum MIF in sepsis.

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