Haruka TodaMiriam Diaz-VarelaJoan Segui-BarberWanlapa RoobsoongBarbara BaroSusana Garcia-SilvaAlicia GalianoMelisa Gualdrón-LópezAnne C.G. AlmeidaMarcelo A.M. BritoGisely Cardoso de MeloIris Aparici-HerraizCarlos Castro-CavadíaWuelton Marcelo MonteiroEva BorràsEduard SabidóIgor C. AlmeidaJakub ChojnackiJavier Martinez-PicadoMaria CalvoPilar ArmengolJaime Carmona-FonsecaMaria Fernanda YasnotRicardo LauzuricaAntonio MarcillaHector PeinadoMary R. GalinskiMarcus V.G. LacerdaJetsumon SattabongkotCarmen Fernandez-BecerraHernando A. del PortilloUniversidad de Córdoba, MonteriaBarcelona Institute of Science and Technology (BIST)Instituto de Salud Global de BarcelonaFundacao de Medicina Tropical do AmazonasUniversitat de Vic - Universitat Central de Catalunya (UVic-UCC)Universidad de AntioquiaUniversitat Pompeu Fabra BarcelonaInstitució Catalana de Recerca i Estudis AvançatsHospital Universitari Germans Trias i PujolFundacao Oswaldo CruzMahidol UniversityCentro Nacional de Investigaciones OncológicasThe University of Texas at El PasoUniversity of ValenciaUniversidade do Estado do AmazonasUniversitat de BarcelonaFundació Institut dInvestigació en Ciències de la Salut Germans Trias i PujolEmory UniversityIrsiCaixa AIDS Research Institute2020-08-252020-08-252020-12-01Nature Communications. Vol.11, No.1 (2020)204117232-s2.0-85085909618https://repository.li.mahidol.ac.th/handle/20.500.14594/57668© 2020, The Author(s). Plasmodium vivax is the most widely distributed human malaria parasite. Previous studies have shown that circulating microparticles during P. vivax acute attacks are indirectly associated with severity. Extracellular vesicles (EVs) are therefore major components of circulating plasma holding insights into pathological processes. Here, we demonstrate that plasma-derived EVs from Plasmodium vivax patients (PvEVs) are preferentially uptaken by human spleen fibroblasts (hSFs) as compared to the uptake of EVs from healthy individuals. Moreover, this uptake induces specific upregulation of ICAM-1 associated with the translocation of NF-kB to the nucleus. After this uptake, P. vivax-infected reticulocytes obtained from patients show specific adhesion properties to hSFs, reversed by inhibiting NF-kB translocation to the nucleus. Together, these data provide physiological EV-based insights into the mechanisms of human malaria pathology and support the existence of P. vivax-adherent parasite subpopulations in the microvasculature of the human spleen.Mahidol UniversityBiochemistry, Genetics and Molecular BiologyChemistryPhysics and AstronomyArticleSCOPUS10.1038/s41467-020-16337-y