SHIGA TOXIN (STX)-PRODUCING ESCHERICHIA COLI STIMULATES NEUTROPHIL INTERLEUKIN-1 BETA (IL-1Β) SECRETION BY A NON-LYTIC CASPASE-1-DEPENDENT MECHANISM

SHIROMIZU, CAROLINA M; SABBIONE, FLORENCIA; VEREERTBRUGGHEN, ALEXIA; ROSATO M; RAMOS, MARÍA V; JANCIC, CAROLINA; FUENTES, FEDERICO; GALLETI, JEREMÍAS; AMARAL MARÍA M; PALERMO, MARINA S; KEITELMAN, IRENE A; TREVANI ANALÍA

Modalidad Virtual

Congreso; Reunión de Sociedades de Biociencias 2021; 2021

SAIC. SAI. AAFE. NANOMED

Shiga toxin (Stx)-producing Escherichia coli (STEC) pathogen establishesnon-invasive intestinal infections that can cause from diarrheaand hemorrhagic colitis to Hemolytic Uremic Syndrome (HUS);a disease that in Argentina is the most common cause of acute renalfailure in early childhood. STEC release Stx in the gut, whichupon translocation to the bloodstream reaches target organs likekidneys and brain, being responsible for HUS pathophysiology. Thistranslocation can be facilitated by mucosal damage and promotedby inflammation.We previously determined that neutrophils (N) isolated from humanperipheral blood release Interleukin-1 beta (IL-1β) when exposed toSTEC but not to bacterial supernatants. Here we investigated therequirements and mechanisms involved in N IL-1β secretion in responseto STEC (serotype O157:H7) by analyzing IL-1β secretion ata multiplicity of infection of 0.5, at which the maximal secretion waspreviously observed. We found that the STEC, an isogenic mutantof STEC lacking the ability to produce Stx, and a non-pathogenicE. coli strain (C600) stimulated IL-1β release. However, IL-1β levelswere significantly higher in response to the pathogenic strainsindependently of their ability to produce Stx (p