ArticlePLoS pathogens2024
Leishmania highjack host lipid body for its proliferation in macrophages by overexpressing host Rab18 and TRAPPC9 by downregulating miR-1914-3p expression.
Article in PLoS pathogens, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
- ApoA1-driven cholesterol efflux and macrophage polarization orchestrate T-cell differentiation towards controlling Leishmania donovani pathogenesis.Scientific reports · 2025Article
- DNA Methylation in macrophages infected withEmerging microbes & infections · 2025Article
- Manipulation of macrophage signaling byVirulence · 2025Review
- The Capsular Polysaccharides GXM and GXMGal fromMicroorganisms · 2025Article
- Scrutinized lipid utilization disrupts Amphotericin-B responsiveness in clinical isolates ofeLife · 2025Article
- VAPA mediates lipid exchange between Leishmania amazonensis and host macrophages.PLoS pathogens · 2025Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Lipids stored in lipid-bodies (LBs) in host cells are potential sources of fatty acids for pathogens. However, the mechanism of recruitment of LBs from the host cells by pathogens to acquire fatty acids is not known. Here, we have found that Leishmania specifically upregulates the expression of host Rab18 and its GEF, TRAPPC9 by downregulating the expression of miR-1914-3p by reducing the level of Dicer in macrophages via their metalloprotease gp63. Our results also show that miR-1914-3p negatively regulates the expression of Rab18 and its GEF in cells. Subsequently, Leishmania containing parasitophorous vacuoles (Ld-PVs) recruit and retain host Rab18 and TRAPPC9. Leishmania infection also induces LB biogenesis in host cells and recruits LBs on Ld-PVs and acquires FLC12-labeled fatty acids from LBs. Moreover, overexpression of miR-1914-3p in macrophages significantly inhibits the recruitment of LBs and thereby suppresses the multiplication of parasites in macrophages as parasites are unable to acquire fatty acids. These results demonstrate a novel mechanism how Leishmania acquire fatty acids from LBs for their growth in macrophages.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.