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Modulation of intracellular calcium concentrations and T cell activation by prickly pear polyphenols

Virginie Aires1, Sylvie Adote, Aziz Hichami

  • 1UPRES Lipides and Nutrition, Université de Bourgogne, Faculté des Sciences de la vie 6, Dijon, France.

Molecular and Cellular Biochemistry
|July 2, 2004
PubMed

Insights

Opuntia ficus indica polyphenolic compounds (OFPC) increase intracellular calcium in T-cells by releasing it from the endoplasmic reticulum and activating CRAC channels. OFPC also suppress T-cell immune responses.

Area of Science:

  • Immunology
  • Cell Biology
  • Pharmacology

Background:

  • Opuntia ficus indica (prickly pear) polyphenolic compounds (OFPC) are known for their potential health benefits.
  • T-cells play a crucial role in the immune system, and their activation involves complex signaling pathways, including calcium influx.
  • Understanding the molecular mechanisms of OFPC action is essential for exploring their therapeutic potential.

Purpose of the Study:

  • To investigate the effect of OFPC on intracellular calcium levels ([Ca2+]i) in human Jurkat T-cells.
  • To elucidate the specific calcium channels and pathways involved in OFPC-induced calcium signaling.
  • To determine the impact of OFPC on T-cell activation markers and immunosuppressive potential.

Main Methods:

  • Human Jurkat T-cells were treated with OFPC in varying calcium concentrations.
  • Inhibitors of calcium release-activated calcium (CRAC) channels (Tyrphostin A9), voltage-dependent calcium channels (lanthanum), L-type calcium channels (nifedipine), and IP3 production (U73122) were used.
  • Thapsigargin (TG) was employed to assess the role of the endoplasmic reticulum (ER) calcium store.
  • Extracellular effects were studied using fatty acid-free bovine serum albumin (BSA).
  • Plasma membrane potential and IL-2 mRNA expression were measured.

Main Results:

  • OFPC triggered a significant increase in [Ca2+]i in Jurkat T-cells, dependent on extracellular calcium.
  • Inhibition of CRAC channels diminished the OFPC-induced calcium response, while lanthanum and nifedipine had no significant effect.
  • OFPC-induced calcium increase was partially dependent on intracellular calcium stores, as indicated by additive effects with TG.
  • U73122 completely abolished the OFPC-induced calcium increase, suggesting IP3 involvement and calcium release from the ER.
  • OFPC acted extracellularly, as BSA reduced the calcium response and reversed OFPC-induced plasma membrane hyperpolarization.
  • OFPC suppressed IL-2 mRNA expression and T-cell blastogenesis.

Conclusions:

  • OFPC induce an increase in intracellular calcium in Jurkat T-cells primarily through the endoplasmic reticulum calcium pool and subsequent activation of CRAC channels.
  • OFPC exhibit immunosuppressive effects on T-cells, evidenced by reduced IL-2 expression and blastogenesis.
  • These findings highlight a novel mechanism of action for OFPC with potential implications for managing T-cell-mediated immune responses.

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