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A Neonatal BALB/c Mouse Model of Necrotizing Enterocolitis
Published on: November 30, 2021
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Cardiac and Inflammatory Necrotizing Enterocolitis in Newborns Are Not the Same Entity
Michaela Klinke1, Hanna Wiskemann1, Benjamin Bay2
1Department of Pediatric Surgery, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Frontiers in Pediatrics
|January 25, 2021
Summary
Necrotizing enterocolitis (NEC) in neonates with cardiac conditions may involve neutrophil extracellular traps (NETs) and ischemia-reperfusion (I/R) injury, differing from inflammatory NEC. This suggests distinct diagnostic and therapeutic approaches for cardiac NEC patients.
Area of Science:
- Neonatal Medicine
- Gastroenterology
- Immunology
Background:
- Necrotizing enterocolitis (NEC) is a severe neonatal condition characterized by intestinal inflammation and necrosis.
- Current diagnostic methods for NEC are often unspecific, complicated by patient comorbidities and multifactorial pathogenesis.
- Neutrophil extracellular traps (NETs) are implicated in ischemia-reperfusion (I/R) injury and inflammation, suggesting a role in NEC development, especially in cardiac patients.
Purpose of the Study:
- To investigate the potential role of NETs in the pathogenesis of NEC, particularly in neonates with cardiac comorbidities.
- To compare NEC patients with and without cardiac disease to identify differences in clinical presentation, laboratory findings, and histological markers.
- To explore potential diagnostic indicators for NEC subtypes based on neutrophil activation and NET formation.
Main Methods:
- Retrospective analysis of 110 surgically verified NEC cases over 10 years.
- Stratification of patients into cardiac NEC (cNEC) and inflammatory NEC (iNEC) groups based on cardiac comorbidities.
- Histological reassessment for neutrophil activation markers (myeloperoxidase, neutrophil elastase) and NET formation (citrullinated histone H3).
Main Results:
- cNEC neonates were significantly older than iNEC neonates (p = 0.005).
- cNEC patients showed significantly increased leukocyte (p = 0.024) and neutrophil (p < 0.001) counts, and altered pH values (p = 0.011) compared to iNEC.
- Histology revealed significantly higher levels of neutrophil elastase (p = 0.012) and citrullinated histone H3 (p = 0.041) in cNEC patients, indicating increased NET formation.
Conclusions:
- Standard NEC diagnostic methods lack specificity.
- Distinct leucocyte and neutrophil profiles in cNEC and iNEC suggest different underlying pathologies.
- Ischemia-reperfusion (I/R) injury, driven by neutrophil activation and NETs formation, is proposed as a primary mechanism in cardiac NEC, contrasting with sepsis-related mechanisms in iNEC.
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