Neutrophil extracellular traps in neonatal necrotizing enterocolitis: from developmental maturation to immunothrombotic injury
- 1Department of Neonatology, Children’s Medical Center, First Hospital of Jilin University
Abstract
Neonatal necrotizing enterocolitis (NEC) is best understood as a syndrome of intestinal necrosis arising in a developmentally susceptible host, with overlapping inflammatory, ischemic, infectious, cardiac-related, and transfusion-associated triggers. Neutrophil extracellular traps (NETs) are extracellular DNA networks decorated with histones, neutrophil elastase, myeloperoxidase, and other granule proteins. They may limit pathogen dissemination, yet persistent NET formation or impaired NET clearance can injure epithelium and microvascular endothelium and amplify immunothrombosis. This review focuses specifically on NETs in NEC. We first condense the general NEC background and then appraise human, animal, and mechanistic evidence with explicit attention to model system, intervention timing, NET detection method, infection burden, and NEC subtype. The neonatal NET-inhibitory factor (nNIF)/NET-maturation window is presented as a testable developmental hypothesis rather than an established quantitative rule. We synthesize biomarker and intervention literature and conclude that the translational question is not simply whether NETs are “good” or “bad”, but which infants, at which disease phase, defined by which combination of formation, clearance, platelet, endothelial, microbial, and imaging signals, may benefit from inhibition, clearance, or preservation of NET function.
Related
- Necrotizing enterocolitis as a disorder of neonatal mucosal immune ecology: from dysbiosis and barrier failure to regulated cell death and precision prevention
- Pharmacokinetics and Efficacy of the FimH Inhibitor Sibofimloc in Preventing Necrotizing Enterocolitis in Preterm Piglets
- Transcriptomics-guided serum podoplanin and interpretable machine learning for early risk stratification of necrotizing enterocolitis in preterm infants
- Divergent Pontine and Cerebellar Pathology in Preterm Infants With Necrotizing Enterocolitis
- Abundant Glomerular Neutrophil Extracellular Traps in C3 Glomerulopathy
BibTeX
@article{chen2026neutrophil,
title = {{Neutrophil extracellular traps in neonatal necrotizing enterocolitis: from developmental maturation to immunothrombotic injury}},
author = {Yang Chen and Mengru Zhu},
journal = {Frontiers in Immunology},
year = {2026},
month = oct,
doi = {10.3389/fimmu.2026.1972426},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1972426/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Neutrophil extracellular traps in neonatal necrotizing enterocolitis: from developmental maturation to immunothrombotic injury
AU - Yang Chen
AU - Mengru Zhu
PY - 2026
DA - 2026/10/20
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.1972426
UR - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1972426/full
AB - Neonatal necrotizing enterocolitis (NEC) is best understood as a syndrome of intestinal necrosis arising in a developmentally susceptible host, with overlapping inflammatory, ischemic, infectious, cardiac-related, and transfusion-associated triggers. Neutrophil extracellular traps (NETs) are extracellular DNA networks decorated with histones, neutrophil elastase, myeloperoxidase, and other granule proteins. They may limit pathogen dissemination, yet persistent NET formation or impaired NET clearance can injure epithelium and microvascular endothelium and amplify immunothrombosis. This review focuses specifically on NETs in NEC. We first condense the general NEC background and then appraise human, animal, and mechanistic evidence with explicit attention to model system, intervention timing, NET detection method, infection burden, and NEC subtype. The neonatal NET-inhibitory factor (nNIF)/NET-maturation window is presented as a testable developmental hypothesis rather than an established quantitative rule. We synthesize biomarker and intervention literature and conclude that the translational question is not simply whether NETs are “good” or “bad”, but which infants, at which disease phase, defined by which combination of formation, clearance, platelet, endothelial, microbial, and imaging signals, may benefit from inhibition, clearance, or preservation of NET function.
SN - 1664-3224
ER -