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Experimental leishmaniasis: the glibenclamide-triggered decrease in parasite growth correlates with changes in

A Ponte-Sucre1, K Figarella, H Moll

  • 1Laboratory of Molecular Physiology, Instituto de Medicina Experimental, Facultad de Medicina, Universidad Central de Venezuela, Caracas. aiponte@reacciun.ve

Immunopharmacology and Immunotoxicology
|November 6, 2001
PubMed
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Glibenclamide (GLIB) treatment of Leishmania-infected macrophages reduces antigen-presenting molecules and promotes a Th1 immune response. This suggests GLIB may help control Th2-biased infections.

Area of Science:

  • Immunology
  • Parasitology
  • Pharmacology

Background:

  • Leishmania parasites are susceptible to glibenclamide (GLIB), a potassium channel blocker.
  • GLIB interacts with adenosine-binding-cassette transporters.
  • Macrophage function as antigen-presenting cells is crucial for immune response modulation.

Purpose of the Study:

  • To investigate the correlation between glibenclamide drug sensitivity in Leishmania amastigotes and alterations in macrophage antigen-presenting cell features.
  • To determine the effect of GLIB on macrophage-mediated immune responses.

Main Methods:

  • BALB/c murine macrophages infected with Leishmania were treated with GLIB.
  • Expression of major histocompatibility complex class II and CD86 (B7-2) was analyzed.

Related Experiment Videos

  • Interleukin-1 secretion was measured.

    • Main Results:

    • GLIB treatment decreased interferon-gamma-stimulated expression of major histocompatibility complex class II and CD86 on macrophages.
    • GLIB reduced interleukin-1 secretion by macrophages.
    • GLIB treatment inhibited Th2 development.

    Conclusions:

    • GLIB alters macrophage function, decreasing key antigen-presenting molecules.
    • GLIB treatment polarizes macrophage function towards a Th1 response.
    • GLIB may be a potential therapeutic agent for modulating immune responses in Leishmania infections.