Abstract
Proteins and glycolipids have been found to be decorated with phosphorylcholine (PC) both in protozoa and nematodes that parasitize humans and animals. PC epitopes can provoke various effects on immune cells leading to an immunomodulation of the host’s immune system that allows long-term persistence of the parasites. So far, only a limited number of PC-modified proteins, mainly from nematodes, have been identified. Infections caused by Leishmania spp. (e.g., L. infantum in southern Europe) affect about 12 million people worldwide and are characterized by a wide spectrum of clinical forms in humans, ranging from cutaneous to fatal visceral leishmaniasis. To establish and maintain the infection, these protozoa are dependent on the secretion of effector molecules into the host for modulating their immune system. In this project, we analyzed the PC modification of L. infantum promastigotes by 2D-gel based proteomics. Western blot analysis with the PC-specific antibody TEPC-15 revealed one PC-substituted protein in this organism, identified as eEF1α. We could demonstrate that the binding of eEF1α to one of its downstream effectors is dependent on its PC-modification. In this study we provide evidence that in this parasite the modification of eEF1α with PC may be essential for its function as an important virulence factor.
Highlights
Leishmaniasis, a vector-borne worldwide-distributed parasitic disease, is caused by dimorphic protozoan flagellates of the genus Leishmania
The L. infantum promastigote protein extract was separated by 2D-gel electrophoresis and
L. infantum promastigote protein extract (see was Figure separated byA2D-gel proteins proteins visualized by Flamingo staining weak electrophoresis blockage in theand iso-electric were visualized by Flamingo staining (see weak blockage due in the focusing focusing (IEF) could be observed in the basic region ofAthe gel probably toiso-electric nucleic acids in the (IEF)
Summary
Leishmaniasis, a vector-borne worldwide-distributed parasitic disease, is caused by dimorphic protozoan flagellates of the genus Leishmania. This organism alternates between two different stages: the promastigote lives extracellular in its vector, the phlebotomine sandfly (Diptera, Psychodidae), and the amastigote resides within the phagolysosome of mononuclear macrophages of mammalian hosts. Leishmaniosis seems to spread because of a combination of Molecules 2017, 22, 2094; doi:10.3390/molecules22122094 www.mdpi.com/journal/molecules and northern Europe [3,4,5]. Leishmaniosis seems to spread because of a combination of factors: environmental/climatic changes, changes, factors related torelated the immune of the hostofand factors: environmental/climatic factors to thestatus immune status thedrug host resistance and drug [6,7]
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