Trated cytoadherence of infected reticulocytes to spleen blood barrier cells of fibroblastic origin (Martin-Jaular et al., 2011). Here, as extracellular vesicles (EVs) play a part in intercellular communication, we hypothesized that plasma-derived EVs from organic vivax infections (PvEVs) signal human spleen fibroblasts facilitating adherence of P. vivax, a reticulocyteprone human malaria parasite. Strategies: Upregulation of ICAM1 as well as other targeted genes upon uptake of PvEVs in human spleen fibroblasts (hSF) was determined by qRT-PCR. Expression of ICAM1 was validated by FACS. NF-kB nuclear translocation evaluation was determined by confocal microscopy. The binding capacity of P. vivax-infected reticulocytes from infections upon uptake of PvEVs was PLK2 web tested right after maturation and purification of frozen estabilates of isolates from Mae Sot (Thailand). P. vivax-infected reticulocytes were incubated with hSF previously stimulated with PvEVs, hEVs or PBS, as well as the variety of binding parasites determined by microscopy. Outcomes: ICAM-1, a recognized receptor for binding of malaria, was specifically upregulated by EVs from infections in a dose-dependent manner at mRNA and protein levels. NF- B was observed each inside the cytoplasm and the nucleus on PARP7 Purity & Documentation non-stimulated and hEVsstimulated hSF, whereas PvEVs stimulation induced nuclear translocation of NF- B on hSF. By comparing the binding of iRBCs to hSF, we final demonstrated significant greater binding to the cells right after uptaken of exosomes from infections. Summary/Conclusion: These final results suggest that circulating exosomes from vivax malaria infections have spleen-tropism signalling spleen fibroblasts to induce ICAM-1 via NF-kB and facilitate adherence of infected reticulocytes. Therefore, unveiling molecular insights of cytoadherence in P. vivax infections. Funding: Funded by Generalitat de Catalunya, Ministerio Espa l de Econom y Competitividad, REDiEX, and Fundaci Ram Areces. HT is recipient of an AGAUR PhD fellowshipOF18.Oxidative pressure alert by extracellular vesicles, in vitro study in ocular drainage program Natalie Lernera, Sofia Schreiber-Avissara and Elie Beit-YannaibaClinical biochemistry and Pharmacology department, Ben-Gurion University, Beer-Sheva, Israel; bBen-Gurion University, Beer-sheva, IsraelJOURNAL OF EXTRACELLULAR VESICLESIntroduction: The ocular drainage program is chronically exposed to oxidative strain (OS) contributing to cataract and primary open angle glaucoma (POAG) improvement. Classical markers of OS were discovered in individuals ocular drainage tissues. The potential of EVs to provide OS alert messages between the aqueous humor generating cells named non pigmented ciliary epithelium (NPCE) end the Trabecular Meshwork (TM) cells draining the aqueous humor was studied. Procedures: NPCE cells were exposed to OS and their released EVs have been collected (Ox-EV). Non-stressed NPCE derived EVs (N-EV) have been utilized as manage. TM cells exposed to the very same OS have been treated with Ox-EV or N-EV and non-stressed TM cells have been use as manage. The EV remedy effect was measured by Nrf2Keap1 signaling pathway modifications such as Nrf2 expression, related antioxidant gene expression, SOD and Catalase activity and TM cell antioxidant capacity. Final results: TM cells exposed to OS caused a considerable 25 reduction in viability. When treated with Ox-EV the viability reduce was abolished. This cell rescue impact was not shown with N-EV therapy. Increase in Nrf2 cytosolic and nucleic expression was identified following TM oxidativ.