IL?17A expressed on neutrophil extracellular traps promotes mesenchymal stem cell differentiation toward bone?forming cells in ankylosing spondylitis

Ankylosing spondylitis (AS) is an inflammatory disease characterized by excessive bone formation. We investigated the presence of neutrophil extracellular traps (NETs) in AS and how they are involved osteogenic capacity marrow mesenchymal stem cells (MSCs) through interleukin-17A (IL-17A). Peripheral neutrophils sera were obtained from patients with active healthy controls. NET formation neutrophil/NET-associated proteins studied using immunofluorescence, immunoblotting, qPCR, ELISA. In vitro co-culture systems structures MSCs isolated controls deployed to examine role NETs differentiation toward cells. Analysis was performed specific staining qPCR. Neutrophils enhanced carrying bioactive IL-17A IL-1?. IL-17A-enriched mediated bone-forming The expression positively regulated Blocking IL-1? signaling on anakinra or dismantling DNase-I disrupted osteogenesis driven IL-17A-bearing NETs. These findings propose a novel AS-related inflammation, linking IL-17A-decorated Moreover, triggers offering additional therapeutic target AS.