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SYSTEMATIC REVIEW article

Front. Pediatr.

Sec. Neonatology

This article is part of the Research TopicAdvancing Perinatal and Pediatric Care: Bridging Basic Research and Clinical PracticeView all 6 articles

The role of myeloid cells in the pathogenesis of necrotizing enterocolitis; a scoping review

Provisionally accepted
  • 1Maternal Fetal Neonatal Institute, Department of Neonatology, Johns Hopkins All Children's Hospital, St. Petersburg, United States
  • 2Division of Neonatal-Perinatal Medicine, Department of Pediatrics, Yale School of Medicine, New Haven, United States

The final, formatted version of the article will be published soon.

Necrotizing enterocolitis (NEC) is a severe gastrointestinal disorder that primarily affects preterm infants, resulting in significant morbidity and mortality. The exact cause of NEC remains unclear, but it is believed to involve a combination of immune dysregulation, intestinal injury, and microbiota imbalance. This scoping review examines existing human and animal studies that explore the role of myeloid cells (neutrophils, monocytes, macrophages, and myeloid-derived suppressor cells (MDSCs) in NEC pathogenesis. A reduction in peripheral blood monocytes, along with increased infiltration of pro-inflammatory monocytes and neutrophils into the intestine, are strongly associated with NEC severity. Immunoregulatory MDSCs may offer protective benefits, and their activity is impaired in preterm infants with NEC. Therapies targeting these immune cells, such as TGF-β2 and lactoferrin, show promise in preclinical models for mitigating inflammation and improving outcomes in infants with NEC. Future research should focus on bringing targeted therapies that modulate myeloid cell immune responses to the bedside as such interventions could help reduce NEC incidence and severity, offering new hope for vulnerable neonates.

Keywords: biomarkers, human milk, Immune dysregulation, Macrophages, Monocytes, myeloid-derived suppressor cells, necrotizing enterocolitis, Neutrophils

Received: 20 Nov 2025; Accepted: 30 Jan 2026.

Copyright: © 2026 Devaris and Olaloye. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Oluwabunmi Olaloye

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