| Literature DB >> 26771494 |
Anthony J Szempruch1, Steven E Sykes1, Rudo Kieft1, Lauren Dennison1, Allison C Becker1, Anzio Gartrell1, William J Martin2, Ernesto S Nakayasu3, Igor C Almeida4, Stephen L Hajduk5, John M Harrington6.
Abstract
Intercellular communication between parasites and with host cells provides mechanisms for parasite development, immune evasion, and disease pathology. Bloodstream African trypanosomes produce membranous nanotubes that originate from the flagellar membrane and disassociate into free extracellular vesicles (EVs). Trypanosome EVs contain several flagellar proteins that contribute to virulence, and Trypanosoma brucei rhodesiense EVs contain the serum resistance-associated protein (SRA) necessary for human infectivity. T. b. rhodesiense EVs transfer SRA to non-human infectious trypanosomes, allowing evasion of human innate immunity. Trypanosome EVs can also fuse with mammalian erythrocytes, resulting in rapid erythrocyte clearance and anemia. These data indicate that trypanosome EVs are organelles mediating non-hereditary virulence factor transfer and causing host erythrocyte remodeling, inducing anemia.Entities:
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Year: 2016 PMID： 26771494 PMCID： PMC4715261 DOI： 10.1016/j.cell.2015.11.051
Source DB: PubMed Journal: Cell ISSN： 0092-8674 Impact factor: 41.582