Promastigotes of the protozoan parasite genus Leishmania are
inoculated into a mammalian host when an infected sand fly takes a
bloodmeal. Following their opsonization by complement, promastigotes
are phagocytosed by macrophages. There, promastigotes differentiate
into amastigotes, the form of the parasite that replicates in the
phagolysosomal compartments of host macrophages. Although the
mechanisms by which promastigotes survive the microbicidal consequence
of phagocytosis remain, for the most part, to be elucidated, evidence
indicates that glycoconjugates play a role in this process. One such
glycoconjugate is lipophosphoglycan, an abundant promastigote surface
glycolipid. Using quantitative electron and confocal laser scanning
microscopy approaches, evidence was provided that L. donovani
promastigotes inhibit phagolysosome biogenesis in a
lipophosphoglycan-dependent manner. This inhibition correlates with an
accumulation of periphagosomal F-actin, which may potentially form a
physical barrier that prevents L. donovani
promastigote-containing phagosomes from interacting with endocytic
vacuoles. Inhibition of phagosome maturation may constitute a strategy
to provide an environment propitious to the promastigote-to-amastigote
differentiation.