HUMAN NEUTROPHILS RESPONSE TO SHIGA TOXIN

SABBIONE, FLORENCIA; MIGLIO, M.; GALLETTI, JEREMÍAS G.; OSTROWSKI, MATÍAS; TREVANI, ANALÍA S.; SHIROMIZU, MAIUMI; F. FUENTES; JANCIC, CAROLINA; PALERMO M; KEITELMAN, IRENE A.; GUZMAN, MAURICIO; GERBER, PEHUÉN PEREYRA; RAMOS M

Mar del Plata

Congreso; LXVI Reunión Anual de la Sociedad Argentina de Inmunología (SAI); 2018

SAI

Shiga-toxin-producing E coli (STEC) infections can cause hemolyticuremic syndrome (HUS), a life-threatening condition. These non-invasive bacteria colonize the intestine where they release the Shigatoxin (Stx) which, after reaching the bloodstream and binding toGb3Cer receptor, causes the characteristic events of the HUS: hemolytic anemia, thrombocytopenia and renal failure. Recently, it hasbeen proposed that Stx is transported in circulation in extracellularvesicles (EV) released by leukocytes and platelets. Neutrophilia is atypical finding in patients with HUS, and elevated neutrophil (PMN)counts are considered a poor prognostic factor. The aim of this research is to determine if PMNs produce EV in response to Stx type2 (Stx2) and to analyze its cytotoxic capacity. 107 PMN isolated fromhuman peripheral blood from healthy donors were incubated withStx2 (0.1 µg/ml) or with vehicle for 4hs. Afterwards, supernatantswere centrifugated at 16000 x g for 30 min to obtain the EV (EV-Stxor EV-Veh). Later, we studied their cytotoxic effect on VERO cells,as a parameter to determine the presence of Stx2 in the EV. Theviability percentage of VERO cells cultured for 48hs with EV-Veh orEV-Stx was 86±3% and 68±2%, respectively (n=6; p