HUMAN NEUTROPHILS SECRETE IL-1B IN RESPONSE TO SHIGA TOXIN (STX)-PRODUCING ESCHERICHIA COLI IN A MECHANISM THAT DEPENDS ON INFLAMMASOME, CASPASE-1 AND OXYGEN REACTIVE SPECIES

SABBIONE F; SHIROMIZU, CM; KEITELMAN I; VERA AGUILA D; VEREERTBRUGGHEN A; PIZZANO M; RAMOS MV; JANCIC C; GALLETTI J; PALERMO M; TREVANI, A

Congreso; Third French-Argentine Immunology Congress ? Reunión Anual Sociedades de Biociencias; 2022

Shiga toxin (Stx)-producing Escherichia coli (STEC) are non-invasivebacteria that colonize the intestine causing diarrhea, hemorrhagiccolitis, and Hemolytic Uremic Syndrome. This disease istriggered by Stx, that translocates to the circulation affecting organslike the kidney. Stx translocation is promoted by inflammation. Asneutrophils (N) are recruited to the intestine upon STEC infections,they might contribute to the gut inflammatory response by secretingInterleukin-1β (IL-1β). We previously determined that STEC (E.coli O157:H7 strain) stimulates IL-1β secretion by human N (HN) bya process that involves N serine proteases (NSP). The aim of thisstudy was to further elucidate the mechanisms that lead to IL-1βsecretion. We determined that an isogenic STEC strain that doesnot produce Stx (ΔSTEC) also stimulates HN IL-1β secretion at asimilar level than STEC does. Moreover, IL-1β response induced byΔSTEC mimicked that induced by STEC; the secretion was higherthe lower the multiplicity of infection (MOI) was, and this effect wasnot due to differences in HN lytic death (n=7; p