Experimental Leishmaniasis: The glibenclamide-triggered decrease in parasite growth correlates with changes in macrophage features.

Abstract

Previous studies from our laboratories revealed the susceptibility of Leishmania sp. to glibenclamide (GLIB), a potassium channel blocker which selectively interacts with adenosine-binding-cassette transporters. In the present work, we analyzed whether the drug sensitivity of intracellular amastigotes correlates with changes in macrophage features that are related to their function as antigen-presenting cells. We provide evidence that in BALB/c murine macrophages, GLIB induced a decrease in the interferon-gamma-stimulated expression of major histocompatibility complex class II molecules and the co-stimulatory molecule CD86 (B7-2). Furthermore, it caused a decrease in the interleukin-1 secretion by macrophages. The data indicate that the treatment with GLIB inhibits the Th2 development and polarizes macrophage functions towards the induction of a protective Th1 response.