Abstract
Leishmaniasis is caused by trypanosomatid protozoa of the genus Leishmania, which infect preferentially macrophages. The disease affects 12 million people worldwide, who may present cutaneous, mucocutaneous or visceral forms. Several factors influence the form and severity of the disease, and the main ones are the Leishmania species and the host immune response. CD100 is a membrane bound protein that can also be shed. It was first identified in T lymphocytes and latter shown to be induced in macrophages by inflammatory stimuli. The soluble CD100 (sCD100) reduces migration and expression of inflammatory cytokines in human monocytes and dendritic cells, as well as the intake of oxidized low-density lipoprotein (oxLDL) by human macrophages. Considering the importance of macrophages in Leishmania infection and the potential role of sCD100 in the modulation of macrophage phagocytosis and activation, we analyzed the expression and distribution of CD100 in murine macrophages and the effects of sCD100 on macrophage infection by Leishmania (Leishmania) amazonensis. Here we show that CD100 expression in murine macrophages increases after infection with Leishmania. sCD100 augments infection and phagocytosis of Leishmania (L.) amazonensis promastigotes by macrophages, an effect dependent on macrophage CD72 receptor. Besides, sCD100 enhances phagocytosis of zymosan particles and infection by Trypanosoma cruzi.
Highlights
Leishmaniasis is a complex of diseases caused by trypanosomatid protozoa of the genus Leishmania, which can be grouped into cutaneous or visceral forms (Alvar et al, 2012)
CD100 Expression Increases in Macrophages During Infection With Leishmania (L.) amazonensis
After demonstrating that Leishmania infection increases macrophage CD100 endogenous levels, we evaluated whether the host cell infection by the parasite was affected by soluble CD100 added to the media
Summary
Leishmaniasis is a complex of diseases caused by trypanosomatid protozoa of the genus Leishmania, which can be grouped into cutaneous or visceral forms (Alvar et al, 2012). The general process of phagocytosis is an essential mechanism of the innate immune response by which phagocytes such as macrophages internalize microorganisms, dead or dying cells, and debris It is an actin-dependent process triggered by the interaction between phagocyte’s receptors and ligands of the particle to be engulfed (May and Machesky, 2001; Underhill and Goodridge, 2012). The effect of sCD100 on oxLDL phagocytosis by macrophage, the main Leishmania host cells, prompted us to study the expression of this molecule and its effects on the phagocytosis of this parasite. We demonstrated that sCD100 effects depend on macrophage CD72, a receptor for CD100 This is the first report of CD100 effect on a parasitic infection, and further studies should address the role of this molecule in animal models of leishmaniasis
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