Systemic inflammation impairs myelopoiesis and interferon type I responses in humans.

ABSTRACT: Systemic inflammatory conditions are classically characterized by an acute hyperinflammatory phase, followed by a late immunosuppressive phase that elevates the susceptibility to secondary infections. Comprehensive mechanistic understanding of these phases is largely lacking. To address this gap, we leveraged a controlled, human in vivo model of lipopolysaccharide (LPS)-induced systemic inflammation encompassing both phases. Single-cell RNA sequencing during the acute hyperinflammatory phase identified an inflammatory CD163⁺SLC39A8⁺CALR⁺ monocyte-like subset (infMono) at 4 h post-LPS administration. The late immunosuppressive phase was characterized by diminished expression of type I interferon (IFN)-responsive genes in monocytes, impaired myelopoiesis and

SUBMITTER: Keramati F 

PROVIDER: S-EPMC12043512 | biostudies-literature | 2025 May

REPOSITORIES: biostudies-literature