Table 3.

Context-dependent interpretation of NET protective versus injurious effects.

Context	Likely dominant NET biology	Potential clinical implication	Key monitoring signals
High bacterial load/translocation risk	NET capture and local antimicrobial concentration; immunothrombotic sealing	Avoid indiscriminate formation blockade; prioritize infection source control and antibiotics	Cultures, lactate, platelet count, perfusion, ultrasound blood flow, NET panel trend
Barrier injured; infection controlled	Persistent histone/protease injury; delayed clearance	Therapeutic window for DNase or short-course selective NET inhibition may exist	Falling bacterial burden but rising cfDNA/H3cit/MPO-DNA, ongoing platelet consumption
Ischemia/cardiac-related phenotype	Endothelial activation, platelet-neutrophil aggregates, microthrombosis	Evaluate perfusion and immunothrombosis nodes; avoid equating with classical inflammatory NEC	Echocardiography/perfusion status, mesenteric Doppler, CD177/platelet aggregates where available
Late/postoperative recovery	Necrosis-derived DNA, ongoing DAMP release, repair-versus-inflammation balance	Clearance and barrier repair may matter more than blocking formation	Enteral tolerance, inflammatory trajectory, renal/pulmonary injury, neurodevelopmental follow-up