2026-04-29T04:52:12Zhttps://repisalud.isciii.es/rest/oai/request

oai:repisalud.isciii.es:20.500.12105/268102025-12-18T12:57:25Zcom_20.500.12105_19586com_20.500.12105_2202col_20.500.12105_19587

00925njm 22002777a 4500 dc Robles-Vera, Iñaki author Jarit-Cabanillas, Aitor author Brandi, Paola author Martínez-López, María author Martínez-Cano, Sarai author Rodrigo-Tapias, Manuel author Femenía-Muiña, Marcos author Redondo-Urzainqui, Ana author Nuñez, Vanesa author González-Correa, Cristina author Moleón, Javier author Duarte, Juan author Conejero, Laura author Mata-Martínez, Pablo author Díez-Rivero, Carmen María author Bergón-Gutiérrez, Marta author Fernández-López, Iván author Gómez, Manuel J author Quintas, Ana author Dopazo, Ana author Sánchez-Cabo, Fátima author Pariente, Esther author Del Fresno, Carlos author Subiza, José Luis author Iborra, Salvador author Sancho, David author 2025-02-11 Impairment of the intestinal barrier allows the systemic translocation of commensal bacteria, inducing a proinflammatory state in the host. Here, we investigated innate immune responses following increased gut permeability upon administration of dextran sulfate sodium (DSS) in mice. We found that Enterococcus faecalis translocated to the bone marrow following DSS treatment and induced trained immunity (TI) hallmarks in bone-marrow-derived mouse macrophages and human monocytes. DSS treatment or heat-killed E. faecalis reprogrammed bone marrow progenitors (BMPs), resulting in enhanced inflammatory responses in vitro and in vivo and protection against subsequent pathogen infections. The C-type lectin receptor Mincle (Clec4e) was essential for E. faecalis-induced TI in BMPs. Clec4e mice showed impaired TI upon E. faecalis administration and reduced pathology following DSS treatment. Thus, Mincle sensing of E. faecalis induces TI that may have long-term effects on pathologies associated with increased gut permeability. Immunity. 2025 Feb 11;58(2):381-396.e9. https://hdl.handle.net/20.500.12105/26810 39848243 Immunity Mincle receptor bone marrow progenitors gut bacterial translocation inflammation macrophages trained immunity Microbiota translocation following intestinal barrier disruption promotes Mincle-mediated training of myeloid progenitors in the bone marrow.