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

## TL;DR

This review explores how myeloid cells contribute to a severe gut disease in preterm infants and suggests immune-targeted therapies could help.

## Contribution

The paper systematically reviews the role of specific myeloid cell types in NEC pathogenesis and highlights potential therapeutic strategies.

## Key findings

- Reduced peripheral blood monocytes and increased intestinal proinflammatory monocytes and neutrophils correlate with NEC severity.
- Immunoregulatory MDSCs may protect against NEC, but their function is impaired in affected preterm infants.
- Therapies targeting TGF-β2 and lactoferrin show promise in preclinical models for reducing NEC inflammation.

## Abstract

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 proinflammatory monocytes and neutrophils into the intestine, are strongly associated with NEC severity. Immunoregulatory MDSCs may provide protective benefits; however, their activity appears impaired in preterm infants with NEC. Therapies targeting these immune pathways, including transforming growth factor-β2 (TGF-β2) and lactoferrin, show promise in preclinical models for mitigating inflammation and improving outcomes in infants with NEC.

Targeting myeloid cell immune responses represents a potential therapeutic strategy in NEC. Future research should focus on translating immune-modulating therapies to clinical practice, as such interventions may reduce NEC incidence and severity and offer new hope for vulnerable neonates.