The sesquiterpene lactone parthenolide inhibits LPS- but not TNF-alpha-induced maturation of human monocyte-derived dendritic cells by inhibition of the p38 mitogen-activated protein kinase pathway

J Allergy Clin Immunol. 2002 Aug;110(2):269-76. doi: 10.1067/mai.2002.126381.

Abstract

Background: Dendritic cells (DCs) are the most potent antigen-presenting cells, and the manipulation of DC maturation provides a strategy for the treatment of allergic and inflammatory diseases.

Objective: In this study we examined the effect of the anti-inflammatory sesquiterpene lactone parthenolide (PTL) on DC maturation induced by LPS or TNF-alpha.

Methods: Human monocyte-derived DCs generated by means of culture with GM-CSF and IL-4 were pretreated with PTL and subsequently stimulated with LPS or TNF-alpha.

Results: PTL inhibited the upregulation of CD80, CD83, CD86, CD40, and MHC class II; the allostimulatory function; the production of TNF-alpha and IL-12; and the downregulation of FITC-labeled dextran uptake in human monocyte-derived DCs stimulated with LPS but not with TNF-alpha. The inhibitory effect of PTL on DC maturation was preceded by inhibition of the phosphorylation of p38 mitogen-activated protein kinase but not the nuclear translocation of NF-kappaB.

Conclusion: These results might offer PTL not only as a promising compound for the treatment of LPS-induced disorders, including sepsis or septic shock, by inhibition of excessive DC maturation but also as a tool to further dissect the signaling pathways involved in DC maturation.

MeSH terms

  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology*
  • Antigens, CD / biosynthesis
  • Antigens, CD1 / biosynthesis
  • B7-1 Antigen / biosynthesis
  • B7-2 Antigen
  • Biological Transport
  • CD40 Antigens / biosynthesis
  • CD83 Antigen
  • Calcium-Calmodulin-Dependent Protein Kinases / metabolism
  • Cell Differentiation
  • Cells, Cultured
  • Dendritic Cells / cytology
  • Dendritic Cells / drug effects*
  • Dendritic Cells / metabolism
  • Down-Regulation
  • Endocytosis / drug effects
  • Histocompatibility Antigens Class II / biosynthesis
  • Humans
  • I-kappa B Proteins / metabolism
  • Immunoglobulins / biosynthesis
  • Interleukin-12 / metabolism
  • Lipopolysaccharides / pharmacology*
  • MAP Kinase Kinase 3
  • MAP Kinase Kinase 6
  • MAP Kinase Signaling System*
  • Membrane Glycoproteins / biosynthesis
  • Mitogen-Activated Protein Kinase Kinases / metabolism
  • Mitogen-Activated Protein Kinases / metabolism*
  • Monocytes / cytology
  • Monocytes / drug effects
  • Monocytes / metabolism
  • NF-kappa B / antagonists & inhibitors*
  • Phosphorylation
  • Protein-Tyrosine Kinases / metabolism
  • Sesquiterpenes / pharmacology*
  • Tumor Necrosis Factor-alpha / metabolism
  • Tumor Necrosis Factor-alpha / pharmacology*
  • Up-Regulation / drug effects
  • p38 Mitogen-Activated Protein Kinases

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • Antigens, CD
  • Antigens, CD1
  • B7-1 Antigen
  • B7-2 Antigen
  • CD1a antigen
  • CD40 Antigens
  • CD86 protein, human
  • Histocompatibility Antigens Class II
  • I-kappa B Proteins
  • Immunoglobulins
  • Lipopolysaccharides
  • Membrane Glycoproteins
  • NF-kappa B
  • Sesquiterpenes
  • Tumor Necrosis Factor-alpha
  • Interleukin-12
  • parthenolide
  • Protein-Tyrosine Kinases
  • Calcium-Calmodulin-Dependent Protein Kinases
  • Mitogen-Activated Protein Kinases
  • p38 Mitogen-Activated Protein Kinases
  • MAP Kinase Kinase 3
  • MAP Kinase Kinase 6
  • MAP2K3 protein, human
  • MAP2K6 protein, human
  • Mitogen-Activated Protein Kinase Kinases