ATAC-Seq based chromatin accessibilty profile of GMP from mice treated with DSS, HK-EF or its excipient.
Inflammatory bowel disease induced by treatment with DSS induce destruction of gut barrier inducing massive bacterial translocation to distal tissue.  Our findings suggest that gut microbiota translocation induces trained immunity in Granulocyte-monocyte progenitors that can underlie pathologies related to low-grade systemic inflammation. The identification of E.faecalis translocation to the bone marrow as a main driver of this effect and its sensing by Mincle receptor in bone marrow progenitors offers potential targets for intervention in pathophysiological settings where gut permeability is altered. Moreover, intravenously and intranasal administration  of HK-EF provided protection against systemic candidiasis in wild-type and Rag1-deficient mice lacking functional lymphocytes, indicative of innate immune-mediated protection. Overall design: Three replicate samples (obtained pooling 2 biological replicates) of Granulocyte-monocyte progenitors from mice treated with DSS or HK-EF or its excipient were used to identify changes in the chromatin accesibility profile using ATAC-seq.