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Cysteinyl leukotrienes induce macrophage inflammatory protein-1 in human monocytes/macrophages

Takashi Ichiyama1, Masanari Hasegawa, Kunio Hashimoto

  • 1Department of Pediatrics, Yamaguchi University Graduate School of Medicine, Yamaguchi, Japan. ichiyama@yamaguchi-u.ac.jp

International Archives of Allergy and Immunology
|September 20, 2008
PubMed
Abstract

Insights

Cysteinyl leukotrienes (CysLTs) stimulate macrophage inflammatory protein (MIP) production in human monocytes via the CysLT(1) receptor and extracellular signal-regulated kinase (ERK) pathway. This finding clarifies inflammatory signaling in monocytes/macrophages.

Area of Science:

  • Immunology
  • Cell Biology
  • Pharmacology

Background:

  • Macrophage inflammatory protein-1alpha (MIP-1alpha) and MIP-1beta are key mediators of inflammation and monocyte recruitment.
  • These chemokines interact with monocytes/macrophages expressing the cysteinyl leukotriene 1 (CysLT(1)) receptor.

Purpose of the Study:

  • To investigate the role of CysLTs in stimulating MIP-1alpha and MIP-1beta production.
  • To elucidate the receptor and intracellular signaling pathways involved in CysLT-induced MIP production.

Main Methods:

  • THP-1 cells and peripheral blood mononuclear cells (PBMCs) were stimulated with CysLTs (LTC(4), LTD(4), LTE(4)).
  • MIP-1alpha and MIP-1beta production and mRNA expression were quantified using ELISA and PCR.
  • The effects of pranlukast (CysLT(1) receptor antagonist) and mitogen-activated protein kinase (MAPK) inhibitors were assessed.

Main Results:

  • CysLTs significantly induced MIP-1alpha and MIP-1beta production in both THP-1 cells and PBMCs.
  • LTD(4) stimulation increased MIP-1alpha and MIP-1beta mRNA levels in THP-1 cells.
  • Pranlukast inhibited LTD(4)-induced MIP production, and an ERK inhibitor attenuated this induction, while JNK and p38 inhibitors had no effect.

Conclusions:

  • CysLTs induce MIP-1alpha and MIP-1beta production in human monocytes/macrophages.
  • This induction is mediated by the CysLT(1) receptor and the extracellular signal-regulated kinase (ERK) signaling pathway.

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