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PurposeNecrotizing enterocolitis (NEC), an in ammatory intestinal disease common in premature infants, has been associated with the development of lung damage. Toll-like receptor 4 has been shown to regulate in ammation in the NEC lungs, however, other important in ammatory mechanisms have not been thoroughly investigated. In addition, we reported that milk-derived exosomes were able to attenuate intestinal injury and in ammation in experimental NEC. This study aims to (i) investigate the role of the NLRP3 in ammasome and NF-κB pathway in regulating lung damage during experimental NEC; and (ii) evaluate the therapeutic potential of bovine milk exosomes in reducing lung in ammation and injury during NEC. Methods NEC was induced by gavage feeding of hyperosmolar formula, hypoxia, and lipopolysaccharide administration in neonatal mice from postnatal days 5-9. Exosomes were obtained by ultracentrifugation of bovine milk and administered during each formula feed. ResultsThe lung of NEC pups showed increased in ammation, tissue damage, NLRP3 in ammasome expression, and NF-κB pathway activation, which were attenuated upon exosome administration. ConclusionOur ndings suggest that the lung undergoes signi cant in ammation and injury following experimental NEC which are attenuated by bovine milk-derived exosomes. This emphasizes the therapeutic potential of exosomes not just on the intestine but also on the lung.

Necrotizing enterocolitis (NEC) is a gastrointestinal disease frequently prevalent in premature neonates. Despite advances in research, there is a lack of accurate, early diagnoses of NEC and the current therapeutic approaches remain exhausted and disappointing. In this review, we have taken a close look at the regenerative medical literature available in the context of NEC treatment. Stem cells from amniotic fluid (AFSC) administration may have the greatest protective and restorative effects on NEC. This review summarizes the potential protection and restoration AFSCs have on NEC-induced intestinal injury while comparing various components within AFSCs like conditioned medium (CM) and extracellular vesicles (EVs). In addition to therapeutic interventions that focus on targeting intestinal epithelial damage and regeneration, a novel discovery that AFSCs act in a Wnt-dependent manner provides insight into this mechanism of protection. Finally, we have highlighted the most important aspects that remain unknown that should be considered to guide future research on the translational application of AFSC-based therapy. We hope that this will be a beneficial frame of reference for the guidance of future studies and towards the clinical application of AFSC and/or its derivatives as a treatment against NEC.

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