Abstract
Lipid droplets (LDs; lipid bodies) are intracellular sites of lipid storage and metabolism present in all cell types. Eukaryotic LDs are involved in eicosanoid production during several inflammatory conditions, including infection by protozoan parasites. In parasites, LDs play a role in the acquisition of cholesterol and other neutral lipids from the host. The number of LDs increases during parasite differentiation, and the biogenesis of these organelles use specific signaling pathways involving protein kinases. In addition, LDs are important in cellular protection against lipotoxicity. Recently, these organelles have been implicated in eicosanoid and specialised lipid metabolism. In this article, we revise the main functions of protozoan parasite LDs and discuss future directions in the comprehension of these organelles in the context of pathogen virulence.
Highlights
Most cells present lipid droplets (LDs), called lipid bodies, which are cytoplasmic organelles involved in lipid compartmentalisation and signaling
These comprise PAT proteins; they support fatty acid (FA), triacylglycerol (TAG) and cholesteryl ester (CE) uptake and are crucial to LD formation de novo in mammalian cells.[2,3,4,5] none of the genes related to PAT protein production have been described in parasites genomes, the LD kinase (LDK) found in trypanosomatids is the only protein in parasitic protozoa known to be responsible for performing a similar function.[6] other organelles take part from the origin until the LD turnover.[7]. The endoplasmic reticulum (ER) provides the structural molecular components necessary for biogenesis, and mitochondria capture the molecules mobilised in LDs for use in metabolic functions[8] (Figure and Table I)
The cell death process triggers the production of LDs in parasites.[18]. Antiparasitic drugs act by interfering with lipid metabolism or inhibiting mitochondrial activity, concomitantly inducing LD formation in trypanosomatids.[19]. Treatment with amiodarone in Leishmania amazonensis was found to lead to degenerative changes mainly in the structure, membrane, and function of mitochondria
Summary
Most cells present lipid droplets (LDs), called lipid bodies, which are cytoplasmic organelles involved in lipid compartmentalisation and signaling. The cell death process triggers the production of LDs in parasites.[18] Antiparasitic drugs act by interfering with lipid metabolism or inhibiting mitochondrial activity, concomitantly inducing LD formation in trypanosomatids.[19] Treatment with amiodarone in Leishmania amazonensis was found to lead to degenerative changes mainly in the structure, membrane, and function of mitochondria. This resulted in cell death marked by a dose-dependent accumulation of LDs, which were near autophagosomes and multivesicular bodies suggesting the induction of LD biogenesis as a result of neutral lipid storage from membrane degradation.[20]. Such strategies are vital for the survival inside the host, allowing them to recruit more resources for their lipid stores and metabolic processes. [13,23] LDs of Trypanosoma cruzi trypomastigotes present large amounts of prostaglandin E2 (PGE2), an important immunomodulatory,(24) showing that demands arising from inflammatory processes trigger LD biogenesis, which likely supports the parasite’s survival during the course of infection
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