Eicosanoid-induced store-operated calcium entry in dendritic cells

Kiyoshi Itagaki1, Beverly E Barton, Thomas F Murphy

  • 1Division of Trauma, Department of Surgery, University of Medicine and Dentistry of New Jersey-New Jersey Medical School, Newark, New Jersey 07101, USA.

Insights

Eicosanoids, such as leukotriene B4 and LTD4, influence dendritic cell (DC) calcium levels by depleting endoplasmic reticulum stores. This finding reveals a novel mechanism for regulating DC function and immune responses.

Area of Science:

  • Immunology
  • Cell Biology
  • Calcium Signaling

Background:

  • Eicosanoids modulate immune cells, including dendritic cells (DCs).
  • Dendritic cell maturation and function are influenced by store-operated calcium entry (SOCE).
  • Intracellular calcium dynamics may mediate eicosanoid effects on DCs.

Purpose of the Study:

  • To investigate the impact of eicosanoids on calcium mobilization in dendritic cells.
  • To determine if eicosanoids affect store-operated calcium entry (SOCE) in DCs.
  • To explore the role of intracellular calcium in eicosanoid-mediated DC function.

Main Methods:

  • Dendritic cells (DCs) were generated from mouse bone marrow.
  • The effects of eicosanoids on intracellular calcium levels and SOCE were measured.
  • RT-PCR was used to identify relevant receptors and ion channels in DCs.

Main Results:

  • Leukotriene B4 (LTB4) and LTD4 depleted calcium from DC endoplasmic reticulum stores.
  • Specific antagonists blocked LTB4 and LTD4-induced calcium store depletion.
  • DCs express receptors for LTB4 and cysteinyl-leukotrienes, along with TRPC and STIM1 proteins involved in SOCE.
  • Prostaglandin E2 (PGE2) did not affect DC calcium mobilization.

Conclusions:

  • Eicosanoids exhibit distinct effects on dendritic cell calcium mobilization.
  • These findings suggest a novel mechanism for regulating DC maturation via calcium signaling.
  • This has significant implications for understanding immune and non-immune inflammatory processes.
Abstract

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