SHIGA TOXIN TYPE 2 ACTIVATES AND ALTERS REPAIR FUNCTIONS OF LIPOPOLYSACCHARIDE-SENSITIZED LATE OUTGROWTH ENDOTHELIAL PROGENITOR CELLS.

PITTALUGA VILLARREAL JR; MENA HA; CASTILLO LA, ; SCHIERLOH L; MARTIRE GRECO D; BIRNBERG WEISS F; SCHATTNER M ; FERNÁNDEZ G. C. ; NEGROTTO, S; LANDONI V.I

Congreso; LXVI Reunion anual de la Sociedad Argentina de Inmunologia; 2018

SAI

Hemolytic Uremic Syndrome (HUS), the main cause of pediatric acute renal failure, is caused by E. coli producing Shiga toxins (Stx) and characterized by massive endothelial damage, which is worsened by inflammation, especially in the presence of bacterial lipopolysaccharides (LPS). Endogenous regeneration of the vessel wall involves local and bone marrow-derived endothelial progenitor cells(EPC) as well as nearby mature endothelial cells (EC). Although Stx toxic effects on mature EC have been widely studied, its action on EPC and angiogenesis remain to be elucidated. We aimed to analyze the effect of Stx alone or in combination with LPS on survival and angiogenic properties of EPC.Human cord blood-derived late-outgrowth EPC and umbilical vein EC were cultured in cytokine-rich growth medium EGM2. Cells were sensitized with LPS for 18 h and then Stx type 2 was added for another 18 h. Nuclear morphology analysis revealed that Stx2, at concentrations that are known to induce mature EC death, had no effect on EPC survival cultured in basic medium (EBM2+ 2% FBS), which undergoapoptosis only after LPS sensitization (p