IMPACT OF EXTRACELLULAR VESICLES RELEASED BY HUMAN NEUTROPHILS TREATED WITH SHIGA TOXIN ON EPITHELIAL AND ENDOTHELIAL RENAL CELLS.

GOMEZ, FERNANDO DANIEL; SHIROMIZU, CAROLINA MAIUMI; PEREZ PAULA S; VEREERTBRUGGHEN, ALEXIA; JANCIC, CAROLINA; ROSATO, MICAELA; AMARAL, MARÍA MARTA; FUENTES, FEDERICO; TREVANI, ANALÍA; PALERMO, MARINA; KEITELMAN, IRENE ANGÉLICA; VERA AGUILAR, DOUGLAS; RAMOS MARÍA VICTORIA; GALLETTI, JEREMÍAS; SABBIONE, FLORENCIA

Mar del Plata

Congreso; https://www.medicinabuenosaires.com/PMID/36368022.pdf; 2022

SAIC. SAFIS. SAI-FAIC.

Shiga toxin (Stx) producing Escherichia coli (STEC) is a non-invasive pathogen that colonises the intestine where it releases the Stx which can reach the blood stream and lead to the Haemolytic Uremic Syndrome (HUS). In HUS neutrophilia is a typical sign and a poor prognosis factor. Previous studies suggest that Stx is transported to target organs like kidneys, in extracellular vesicles (EV) generated by blood cells. The aim of this study was to determine if neutrophils (N) produce EV in response to Stx (VE-Stx) and their impact on the viability and cytokine production by primary human glomerular endothelial cells (HGEC) and renal epithelial cells (HK-2 cells). Human N (106) isolated from peripheral blood were treated with purified Stx2 (100 ng/ml), heat-inactivated Stx2 (StxØ) or vehicle (C) for 4 h and EV released were isolated by differential centrifugation. By both CLSM (n=4) and detection of CD63 expression by western blot (n=6), we determined that N release EV in all the conditions studied. By employing the VERO cell line susceptible to Stx, we observed that EV-Stx but not EV-StxØ or EV-C significantly reduced cell viability (n=10; p