Fetal pulmonary inflammation, as measured by increased cord blood levels of sE-selectin and neutrophil counts in the tracheal aspirate at birth, may be a risk factor for the development of new BPD in preterm infants. These results support the hypothesis that the lung injury responsible for new BPD in preterm infants can begin in the prenatal period and could be associated with a fetal pulmonary inflammation.

Purpose: ROP is the leading cause of blindness in the children. Inflammation is being highlighted as the major factor for the morbidity of prematurity. We intended to investigate the effect of neonatal systemic inflammation on the retinal angiogenesis in newborn rats and to show the role of inflammation in the retinopathy of prematurity. Method: Systemic inflammation was induced by the pre‐ and post‐natal intraperitoneal injections of lipopolysaccharide (LPS) in neonatal rats. Enucleation and retinal separation was performed at 1 and 2 post‐natal weeks. Analyses on morphology of retinal vessels, recruited immune cells, change of inflammatory cytokines were assessed with immunofluorescence, FACS and RT‐PCR. Result: Administration of LPS postnatlly, not prenatally, induced inflammation in the retina with recruitment of CD11c positive cells and increased expression of a set of inflammatory cytokine genes. Postnatal LPS administration also suppressed retinal vessel development and deranged the retinal vascular structures combined with abnormal vascular tuft formation that resembles features of retinopathy of prematurity. Conclusion: Neonatal systemic inflammation alters the normal development of retinal vessels by inducing retinal inflammation. Our model of systemic inflammation‐induced abnormal development of retinal vasculature can be a novel experimental model of retinopathy of prematurity.