Prenatal low-dose endotoxin exposure prolongs intestinal epithelial activation after birth and contributes to necrotizing enterocolitis

Prenatal exposure to low-dose endotoxin primes the neonatal intestine for prolonged inflammatory activation after birth by upregulating IRAK-1 via GSK3β signaling. This disrupted epithelial response increases susceptibility to necrotizing enterocolitis in experimental models, suggesting prenatal inflammatory exposures may be a risk factor for NEC development.