Human neutrophils secrete IL-1βin response to Shiga toxin (STX)-producing Escherichia coli in a mechanism that depends on inflammasome, caspase-1 and oxygen reactive species

SABBIONE, FLORENCIA; SHIROMIZU, CAROLINA MAIUMI; KEITELMAN, IRENE ANGÉLICA; VERA AGUILAR, DOUGLAS; VEREERTBRUGGHEN, ALEXIA; PIZZANO, MANUELA; RAMOS, MARÍA VICTORIA; JANCIC, CAROLINA CAROLINA; GALLETTI, JEREMÍAS G.; PALERMO, MARINA; ANALÍA, TREVANI SILVINA

Mar del Plata

Congreso; Reunión de Sociedades de Biociencias 2022. LXX Reunión Anual de la Sociedad Argentina de Inmunología y 3er Congreso Franco-Argentino de inmunología; 2022

Shiga toxin (Stx)-producing Escherichia coli (STEC) are non-invasive bacteria that colonize the intestine causing diarrhea, hemorrhagic colitis, and Hemolytic Uremic Syndrome. This disease is triggered by Stx, that translocates to the circulation affecting organs like the kidney. Stx translocation is promoted by inflammation. As neutrophils (N) are recruited to the intestine upon STEC infections, they might contribute to the gut inflammatory response by secreting Interleukin-1β (IL-1β). We previously determined that STEC (E. coli O157:H7 strain) stimulates IL-1β secretion by human N (HN) by a process that involves N serine proteases (NSP). The aim of this study was to further elucidate the mechanisms that lead to IL-1β secretion. We determined that an isogenic STEC strain that does not produce Stx (ΔSTEC) also stimulates HN IL-1β secretion at a similar level than STEC does. Moreover, IL-1β response induced by ΔSTEC mimicked that induced by STEC; the secretion was higher the lower the multiplicity of infection (MOI) was, and this effect was not due to differences in HN lytic death (n=7; p