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

SHIROMIZU, CAROLINA MAIUMI; SABBIONE, FLORENCIA; VEREERTBRUGGHEN, ALEXIA; ROSATO, MICAELA; RAMOS, MARÍA VICTORIA; JANCIC, CAROLINA CRISTINA; FUENTES, FEDERICO; GALLETTI, JEREMÍAS; AMARAL, MARÍA MARTA; PALERMO, MARINA; KEITELMAN, IRENE ANGÉLICA; ANALÍA, TREVANI SILVINA

Congreso; Reunion de Sociedades de Biociencias 2021; 2021

SAI-SAIC-AAFE-NANOMEDAR

Shiga toxin (Stx)-producing Escherichia coli (STEC) pathogen establishes non-invasive intestinal infections that can cause from diarrhea and hemorrhagic colitis to Hemolytic Uremic Syndrome (HUS); a disease that in Argentina is the most common cause of acute renal failure in early childhood. STEC release Stx in the gut, which upon translocation to the bloodstream reaches target organs like kidneys and brain, being responsible for HUS pathophysiology. This translocation can be facilitated by mucosal damage and promoted by inflammation. We previously determined that neutrophils (N) isolated from human peripheral blood release Interleukin-1 beta (IL-1β) when exposed to STEC but not to bacterial supernatants. Here we investigated the requirements and mechanisms involved in N IL-1β secretion in response to STEC (serotype O157:H7) by analyzing IL-1β secretion at a multiplicity of infection of 0.5, at which the maximal secretion was previously observed. We found that the STEC, an isogenic mutant of STEC lacking the ability to produce Stx, and a non-pathogenic E. coli strain (C600) stimulated IL-1β release. However, IL-1β levels were significantly higher in response to the pathogenic strains independently of their ability to produce Stx (p