IL-10 DEFICIENCY MODULATES INFLAMMATORY RESPONSE AND ANTI-INFLAMMATORY MEDIATORS IN A MURINE MODEL OF HEMOLYTIC UREMIC SYNDROME (HUS)

CATALINA ALBA SOTO; ANDREA BRUBALLA; MARINA PALERMO; GONZALO EZEQUIEL PINEDA; BÁRBARA REARTE; MARTÍN ISTURIZ; MARLINA OLYISSA CÓRDOBA MORENO; ROMINA FERNANDEZ BRANDO; MARÍA VICTORIA RAMOS

Buenos Aires

Congreso; Reunión Conjunta de Sociedades de Biociencia 2017; 2017

SAIC - SAI - SAB - SAIB - SAH - SAB - SAFE - SAFIS - SAP - SAA

Hemolytic Uremic Syndrome is a disease triggered by Shiga toxin(Stx) characterized by hemolytic anemia, thrombocytopenia and renalfailure. The concomitant inflammatory response mediated mainlyby neutrophils (PMN) is essential to HUS.Previously we demonstrated that mice lacking IL-10 (IL-10-/-) hada higher survival after Stx2 and a delayed neutrophilia compared tocontrol mice (wt). The aim of this work was to determine the mechanismsinvolved in IL-10-/- protection against Stx2.Before and 3h, 24h, 48h and 72h after administration of 1LD100 of Stx2 e.v, IL-10-/- and wt mice were sacrificed. Plasma was collectedto evaluate creatinine as an indicator of renal damage and corticosteronesince IL-10 regulates glucocorticoid synthesis at the level ofthe adrenal gland. Peripheral PMN were detected as Ly6G+CD11b+cells and CXCR2 and CD62L expression was analyzed by FACS.Even though creatinine levels (mg/dl) were increased at 72h inboth strains, IL-10-/- showed reduced levels comparted to wt suggestingreduced renal damage (Wt0h: 0.5±0.1; Wt72h: 1,4±0,1*;IL-10-/-0h: 0.4±0.1; IL-10-/-72h: 0.9±0.1*#, *