The Role of the Interleukin-1 Family in Complications of Prematurity

Preterm birth is a major contributor to neonatal morbidity and mortality. Complications of prematurity such as bronchopulmonary dysplasia (BPD, affecting the lung), pulmonary hypertension associated with BPD (BPD-PH, heart), white matter injury (WMI, brain), retinopathy of prematurity (ROP, eyes), necrotizing enterocolitis (NEC, gut) and sepsis are among the major causes of long-term morbidity in infants born prematurely. Though the origins are multifactorial, inflammation and in particular the imbalance of pro- and anti-inflammatory mediators is now recognized as a key driver of the pathophysiology underlying these illnesses. Here, we review the involvement of the interleukin (IL)-1 family in perinatal inflammation and its clinical implications, with a focus on the potential of these cytokines as therapeutic targets for the development of safe and effective treatments for early life inflammatory diseases.

Automated summary

Preterm birth is a major cause of neonatal morbidity and mortality, with complications such as BPD, BPD-PH, WMI, ROP, NEC, and sepsis. Inflammation, particularly the imbalance of pro- and anti-inflammatory mediators, plays a key role in the pathophysiology of these diseases. This review focuses on the involvement of the IL-1 family in perinatal inflammation and its clinical implications, highlighting the potential of these cytokines as therapeutic targets for early life inflammatory diseases.