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Target intelligence / Profile preview
Neutrophil extracellular trap (NET) DNA consists of extracellular chromatin fibers released by neutrophils to capture and kill pathogens. While essential for innate immunity, the persistence of these DNA scaffolds can trigger harmful inflammatory responses and tissue damage. In the context of cystic fibrosis, NET DNA significantly contributes to the high viscosity of pulmonary secretions, leading to airway obstruction. Furthermore, NET DNA serves as a scaffold for platelet aggregation and fibrin deposition, promoting immunothrombosis in cardiovascular diseases. It also plays a role in autoimmune diseases like systemic lupus erythematosus, where it acts as a source of autoantigens. Therapeutic intervention typically involves the use of recombinant human deoxyribonuclease I (rhDNase), which enzymatically cleaves the DNA backbone. This degradation reduces the physical viscosity of mucus and dismantles the pro-thrombotic and pro-inflammatory lattice. Emerging research also explores the role of NET DNA in shielding tumor cells from the immune system and promoting metastatic niche formation.
Enzymatic hydrolysis of phosphodiester bonds within the DNA backbone, leading to the degradation of the extracellular chromatin scaffold and reduction of fluid viscosity.
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