Preventing inflammation- induced injury in the central nervous respiratory system of preterm newborns

Preterm birth is the leading cause of neonatal mortality and morbidity, with respiratory dysfunction being a major contributor. Central nervous system (CNS) respiratory centers, essential for generating breathing, are highly susceptible to inflammatory injury. This thesis investigated the structural and functional consequences of common perinatal inflammatory insults and mechanical ventilation on these centers. Using in utero ventilation (IUV) and endotoxin exposure models, we demonstrated that even short-term ventilation induces peripheral and neuroinflammation, while pulmonary endotoxin drives brainstem injury. Interleukin-1 emerged as a key biomarker of CNS inflammation. Furthermore, IL-1 receptor antagonist (anakinra) effectively attenuated endotoxin-induced injury, highlighting IL-1 modulation as a promising therapeutic strategy for preterm infants.