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- W4313369030 abstract "Abstract Visceral leishmaniasis (VL) is a potentially fatal disease caused by Leishmania donovani or L. infantum. Parasites reside quiescently in macrophages (Mϕ) but dramatically affect systemic immune responses. These Mϕs, like most eukaryotic cells, release small, protein- and RNA-laden extracellular vesicles called exosomes, which facilitate intercellular communication. We hypothesized exosomes released from infected Mϕs mediate some systemic immune changes in VL. If correct, exoproteomes of infected Mϕs must differ from uninfected Mϕs. Monocyte derived Mϕs (MDMs) from 4 healthy human donors were infected with L. infantum and extracellular parasites removed. Exosomes were collected and exoproteomes were isotope labeled and identified by LC-MS/MS. Data were exported in MaxQuant 1.6.3.3, and analyzed with Perseus 1.6.2.3. After filtering for quality and for proteins found in all 5 technical replicates of at least one group, 244 proteins were quantified. Pairwise comparison revealed significant differences between donors (FDR 0.05, S0=1), and between infected and uninfected states. 2-way ANOVA (p<0.05) revealed 100 proteins differed significantly by infection status, including histone proteins, HSP-70, Prosaposin, Lipoprotein lipase, CD36, Galectin-9 and several histocompatibility regions and antibody constant chains. The data are reflective of dysregulated lipid metabolism known to occur in visceral leishmaniasis. These findings highlight a need to investigate Heat Shock proteins, lipid metabolic pathway proteins, histocompatibility antigens, and histones in extracellular vesicles as potential contributors to the immune dysregulation observed during leishmaniasis." @default.
- W4313369030 created "2023-01-06" @default.
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- W4313369030 date "2020-05-01" @default.
- W4313369030 modified "2023-09-27" @default.
- W4313369030 title "Proteomic analysis of exosomes released from <i>Leishmania</i> infected macrophages" @default.
- W4313369030 doi "https://doi.org/10.4049/jimmunol.204.supp.156.19" @default.
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