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Lactoferrin down-regulates the LPS-induced cytokine production in monocytic cells via NF-kappa B

Liliana Håversen1, Bertil G Ohlsson, Mirjana Hahn-Zoric

  • 1Department of Clinical Bacteriology, University of Göteborg, Guldhedsgatan 10, S-41346 Göteborg, Sweden. liliana.ceafalau@microbio.gu.se

Cellular Immunology
|March 27, 2003
PubMed

Insights

Milk lactoferrin (LF) reduces inflammatory cytokine production in immune cells by interfering with the NF-kappa B pathway. This finding supports LF

Area of Science:

  • Immunology
  • Biochemistry
  • Molecular Biology

Background:

  • Lactoferrin (LF), a milk glycoprotein, plays a role in host defense.
  • Previous studies demonstrated LF's anti-infectious and anti-inflammatory effects in vivo.
  • LF was previously shown to inhibit LPS-induced IL-6 secretion in THP-1 cells.

Purpose of the Study:

  • To investigate LF's capacity to inhibit cytokine mRNA expression.
  • To explore the involvement of nuclear transcription factor kappa B (NF-kappa B) in LF's mechanism of action.
  • To expand on previous findings regarding LF's anti-inflammatory properties in monocytic cell lines.

Main Methods:

  • Utilized semiquantitative RT-PCR to measure cytokine mRNA expression (TNF-alpha, IL-1 beta, IL-6, IL-8).
  • Employed ELISA to quantify secreted cytokine levels.
  • Investigated NF-kappa B activation using electrophoretic mobility shift assay (EMSA).
  • Visualized LF internalization and localization via immunostaining and immunofluorescence.

Main Results:

  • LF treatment significantly reduced mRNA expression and secretion of TNF-alpha, IL-1 beta, IL-6, and IL-8 in THP-1 cells.
  • LF also down-regulated IL-10 secretion in Mono Mac 6 cells.
  • LF was internalized into monocytic cells and localized in the nucleoli.
  • EMSA analysis revealed that LF decreased LPS-induced NF-kappa B binding to the TNF-alpha promoter.

Conclusions:

  • Lactoferrin effectively down-regulates LPS-induced cytokine production in monocytic cells.
  • The inhibitory mechanism of LF involves interference with NF-kappa B activation.
  • These findings highlight LF's potential as an anti-inflammatory agent targeting the NF-kappa B pathway.

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