Introduction 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. Methods 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. Results 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. Conclusions 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.
Devaris et al. (Fri,) studied this question.