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Differences in human macrophage receptor usage, lysosomal fusion kinetics and survival between logarithmic and metacyclic Leishmania infantum chagasi promastigotes
Journal article   Open access   Peer reviewed

Differences in human macrophage receptor usage, lysosomal fusion kinetics and survival between logarithmic and metacyclic Leishmania infantum chagasi promastigotes

Norikiyo Ueno, Carol L Bratt, Nilda E Rodriguez and Mary E Wilson
Cellular microbiology, Vol.11(12), pp.1827-1841
12/2009
DOI: 10.1111/j.1462-5822.2009.01374.x
PMCID: PMC2788030
PMID: 19702651
url
https://doi.org/10.1111/j.1462-5822.2009.01374.xView
Published (Version of record) Open Access

Abstract

The obligate intracellular protozoan, Leishmania infantum chagasi (Lic) undergoes receptor-mediated phagocytosis by macrophages followed by a transient delay in phagolysosome maturation. We found differences in the pathway through which virulent Lic metacyclic promastigotes or avirulent logarithmic promastigotes are phagocytosed by human monocyte-derived macrophages (MDMs). Both logarithmic and metacyclic promastigotes entered MDMs through a compartment lined by the third complement receptor (CR3). In contrast, many logarithmic promastigotes entered through vacuoles lined by mannose receptors (MR) whereas most metacyclic promastigotes did not (P < 0.005). CR3-positive vacuoles containing metacyclic promastigotes stained for caveolin-1 protein, suggesting CR3 localizes in caveolae during phagocytosis. Following entry, the kinetics of phagolysosomal maturation and intracellular survival also differed. Vacuoles containing metacyclic parasites did not accumulate lysosome-associated membrane protein-1 (LAMP-1) at early times after phagocytosis, whereas vacuoles with logarithmic promastigotes did. MDMs phagocytosed greater numbers of logarithmic than metacyclic promastigotes, yet metacyclics ultimately replicated intracellularly with greater efficiency. These data suggest that virulent metacyclic Leishmania promastigotes fail to ligate macrophage MR, and enter through a path that ultimately enhances intracellular survival. The relatively quiescent entry of virulent Leishmania spp. into macrophages may be accounted for by the ability of metacyclic promastigotes to selectively bypass deleterious entry pathways.
Mannose-Binding Lectins - metabolism Humans Virulence Leishmaniasis, Visceral - immunology Leishmania infantum - physiology Macrophages - parasitology Caveolae - parasitology Lectins, C-Type - metabolism Lysosomes - metabolism Macrophage-1 Antigen - metabolism Leishmaniasis, Visceral - parasitology Cell Culture Techniques Host-Parasite Interactions Macrophages - immunology Leishmania infantum - pathogenicity Caveolae - metabolism Receptors, Cell Surface - metabolism Cathepsin D - metabolism Leishmaniasis, Visceral - metabolism Lysosomes - parasitology Caveolin 1 - metabolism Macrophages - metabolism Animals Lysosomal-Associated Membrane Protein 1 - metabolism Phagocytosis

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