Involvement of lipids from Leishmania braziliensis promastigotes and amastigotes in macrophage activation

Carfagna, Ivanna Emilce; Penas, Federico Nicolás; Bott, Emanuel; Lammel, E.; Goren, Nora; Belaunzarán, María Laura; Giménez, Guadalupe Ruiz

doi:10.1016/j.molimm.2020.06.023

Cited by 3 publications

(3 citation statements)

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“…AMPK activity helped Leishmania proliferation (26), while it hindered the growth of T. cruzi (62,104). An increase in phosphocholines was observed in Leishmania and T. cruzi infection, while a depletion of overall phosphocholines was observed for T. brucei, with just specific phosphocholines being increased (27,43,61). The bloodstream form of T. brucei metabolizes amino acids (76).…”

Section: Discussionmentioning

confidence: 99%

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Tryp-ing Up Metabolism: Role of Metabolic Adaptations in Kinetoplastid Disease Pathogenesis

Parab

McCall

2021

Infect Immun

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Today, more than a billion people – one-sixth of the world’s population – are suffering from neglected tropical diseases. Human African trypanosomiasis, Chagas disease, and leishmaniasis are neglected tropical diseases caused by protozoan parasites belonging to the genera Trypanosoma and Leishmania. About half a million people living in tropical and subtropical regions of the world are at risk of contracting one of these three infections. Kinetoplastids have complex life cycles with different morphologies and unique physiological requirements at each lifecycle stage. This review covers the latest findings on metabolic pathways impacting disease pathogenesis of kinetoplastids within the mammalian host. Nutrient availability is a key factor shaping in vivo parasite metabolism; thus, kinetoplastids display significant metabolic flexibility. Proteomic and transcriptomic profiles show that intracellular trypanosomatids are able to switch to an energy-efficient metabolism within the mammalian host system. Host metabolic changes can also favor parasite persistence, and contribute to symptom development, in a location-specific fashion. Ultimately, targeted and untargeted metabolomics studies have been a valuable approach to elucidate the specific biochemical pathways affected by infection within the host, leading to translational drug development and diagnostic insights.

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Section: Discussionmentioning

confidence: 99%

“…Parasite metabolites can also affect immune responses; for example, lipids from L. braziliensis amastigotes stimulate nitric oxide production (43). Increased LPC levels worsen dendritic cell infection with L. major by decreasing inducible nitric oxide synthase (iNOS) expression (44).…”

Section: Leishmaniasesmentioning

confidence: 99%

Tryp-ing Up Metabolism: Role of Metabolic Adaptations in Kinetoplastid Disease Pathogenesis

Parab

McCall

2021

Infect Immun

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“…It was reported that lipid extracts from Trypanosoma cruzi amastigotes induced a pro-inflammatory response in murine peritoneal macrophages, as evidenced by increased formation of lipid bodies, COX2 expression, TNF-alpha secretion, and NO release (Bott et al, 2018). Similarly, lipid extracts from L. braziliensis amastigotes were shown to favor M1 macrophage polarization relative to the M2 phenotype whereas promastigotes conversely favored the M2 phenotype with increased arginase activity, IL10 secretion and M2 mRNA markers (Carfagna et al, 2020). It is well-known that PUFA play a key role in inflammatory processes and their resolution through the production of lipid mediators, the interaction with cell surface receptors or the regulation of inflammatory gene expression.…”

Section: Introductionmentioning

confidence: 99%

Enriched PUFA environment of Leishmania infantum promastigotes promotes the accumulation of lipid mediators and favors parasite infectivity towards J774 murine macrophages

Leroux

Messaoud

Luquain-Costaz

et al. 2022

Lipids

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Leishmania parasites are the causative agents of visceral or cutaneous leishmaniasis in humans and of canine leishmaniosis. The macrophage is the predilected host cell of Leishmania in which the promastigote stage is transformed into amastigote. We previously showed changes in the fatty acid composition (FA) of lipids in two strains of Leishmania donovani upon differentiation of promastigote to amastigote, including increased proportions of arachidonic acid (AA) and to a less extent of docosahexaenoic acid (DHA). Here, we carried out supplementation with AA or DHA on two Leishmania infantum strains, a visceral (MON-1) and a cutaneous (MON-24), to evaluate the role of these FA in parasite/macrophage interactions. The proportions of AA or DHA in total lipids were significantly increased in promastigotes cultured in AA-or DHAsupplemented media compared to controls. The content of FA-derived oxygenated metabolites was enhanced in supplemented strains, generating especially epoxyeicosatrienoic acids (11,(12)(13)(14) and hydroxyeicosatetraenoic acids (5-and 8-HETE) from AA, and hydroxydocosahexaenoic acids (14and 17-HDoHE) from DHA. For both MON-1 and MON-24, AA-supplemented promastigotes showed higher infectivity towards J774 macrophages as evidenced by higher intracellular amastigote numbers. Higher infectivity was observed after DHA supplementation for MON-24 but not MON-1 strain. ROS production by macrophages increased upon parasite infection, but only minor change was observed between control and supplemented parasites. We

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Balancing de novo synthesis and salvage of lipids by Leishmania amastigotes

Zhang

2021

Current Opinion in Microbiology

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Involvement of lipids from Leishmania braziliensis promastigotes and amastigotes in macrophage activation

Cited by 3 publications

References 38 publications

Tryp-ing Up Metabolism: Role of Metabolic Adaptations in Kinetoplastid Disease Pathogenesis

Tryp-ing Up Metabolism: Role of Metabolic Adaptations in Kinetoplastid Disease Pathogenesis

Enriched PUFA environment of Leishmania infantum promastigotes promotes the accumulation of lipid mediators and favors parasite infectivity towards J774 murine macrophages

Balancing de novo synthesis and salvage of lipids by Leishmania amastigotes

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