Bovine milk-derived exosomes attenuate NLRP3 inflammasome and NF-κB signaling in the lung during neonatal necrotizing enterocolitis
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In brief
In brief
Experimental study demonstrates that necrotizing enterocolitis triggers significant lung inflammation and injury in neonatal mice through NLRP3 inflammasome and NF-κB pathway activation. Bovine milk-derived exosomes successfully attenuated both intestinal and pulmonary damage, suggesting a novel therapeutic approach for protecting multiple organ systems in premature infants with NEC.
Written by the GCMD Library team from the article.
Abstract
Purpose
Necrotizing enterocolitis (NEC), an inflammatory intestinal disease common in premature infants, has been associated with the development of lung damage. Toll-like receptor 4 has been shown to regulate inflammation in the NEC lungs, however, other important inflammatory mechanisms have not been thoroughly investigated. In addition, we reported that milk-derived exosomes were able to attenuate intestinal injury and inflammation in experimental NEC. This study aims to (i) investigate the role of the NLRP3 inflammasome and NF-κB pathway in regulating lung damage during experimental NEC; and (ii) evaluate the therapeutic potential of bovine milk exosomes in reducing lung inflammation 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.
Results
The lung of NEC pups showed increased inflammation, tissue damage, NLRP3 inflammasome expression, and NF-κB pathway activation, which were attenuated upon exosome administration.
Conclusion
Our findings suggest that the lung undergoes significant inflammation 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.