Mitochondrial activity promotes neutrophil degranulation and endothelial dysfunction in systemic infections

ABSTRACT: Neutrophils are essential for defense against pathogens but excessive activation in systemic infections can drive immunopathology. We show that neutrophil degranulation can induce endothelial dysfunction via degradation of the glycocalyx and increase of endothelial permeability. To identify targetable pathways regulating neutrophil degranulation in severe inflammation, we compared the proteomes of neutrophils isolated from patients with severe malaria and sepsis. We found significant upregulation of mitochondrial pathways, which was accompanied by increased rates of mitochondrial respiration and was linked to neutrophil immaturity. Malaria induced mitochondrial fusion and networking, while sepsis was associated with mitochondrial biogenesis. Immature neutrophils in both infections produced

SUBMITTER: Przemyslaw Zakrzewski 

PROVIDER: S-SCDT-10_1038-S44321-026-00453-1 | biostudies-other |

REPOSITORIES: biostudies-other