Long-term immune reprogramming of classical monocytes with altered ontogeny mediates enhanced lung injury in sepsis survivors.

ABSTRACT: Patients who survive sepsis are predisposed to new hospitalizations for respiratory failure, but the underlying mechanisms are unknown. Using a murine model in which prior sepsis predisposes to enhanced lung injury, we previously discovered that classical monocytes persist in the lungs after long-term recovery from sepsis and exhibit enhanced cytokine expression after secondary challenge with intra-nasal lipopolysaccharide. Here, we hypothesized that immune reprogramming of post-sepsis monocytes and altered ontogeny predispose to enhanced lung injury. Monocyte depletion and/or adoptive transfer was performed three weeks and three months after sepsis. Monocytes from post-sepsis mice were necessary and sufficient for enhanced LPS-induced lung injury and promoted neutrophil degranulation. Pri

SUBMITTER: Denstaedt SJ 

PROVIDER: S-EPMC12139851 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature