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Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
Published on: November 20, 2015
Perinatal infection, inflammation, and retinopathy of prematurity
1Division of Newborn Medicine, Box 44, Floating Hospital for Children at Tufts Medical Center, 800 Washington St, Boston, MA 02111-1526, USA. jlee9@tuftsmedicalcenter.org
Insights
Perinatal infection and inflammation increase the risk of retinopathy of prematurity (ROP) in premature infants. Targeting inflammation may help prevent ROP by sensitizing the retina to oxygen-related damage.
Area of Science:
- Neonatal ophthalmology
- Perinatal medicine
- Inflammatory disease research
Background:
- Retinopathy of prematurity (ROP) is a significant cause of vision impairment in premature infants.
- Established risk factors include extremely low gestational age and oxygen exposure (phases I and II).
- Emerging evidence links perinatal infection/inflammation to increased ROP risk.
Purpose of the Study:
- To review current data on the association between perinatal infection/inflammation and ROP.
- To explore potential mechanisms linking inflammation to ROP pathogenesis.
- To highlight the role of inflammation as a potential 'pre-phase' in ROP development.
Main Methods:
- Literature review of recent studies on ROP risk factors.
- Analysis of proposed pathophysiological pathways involving infection, inflammation, and oxidative stress.
- Synthesis of evidence supporting a multi-stage model of ROP development.
Main Results:
- Perinatal infection/inflammation is associated with a higher risk of developing ROP.
- Inflammation may directly affect the developing retina or modify oxygen-induced damage.
- Systemic inflammation (prenatal, perinatal, postnatal) may sensitize the retina, creating a 'pre-phase' for ROP.
Conclusions:
- Inflammation plays a crucial role in ROP pathogenesis, potentially acting as a sensitizing 'pre-phase'.
- Understanding these inflammatory mechanisms is key to developing new preventative strategies.
- Targeting inflammatory responses could reduce ROP incidence in extremely low gestational age newborns.
Abstract:
The major known risk factors for retinopathy of prematurity (ROP) are extremely low gestational age, exposure to high levels of oxygen early after birth (phase I) and relatively lower oxygen levels later (phase II). In this review, we summarize recent data suggesting that exposure to perinatal infection/inflammation is associated with an increased risk for ROP. Part of this effect might be due to direct exposure of the developing retina to circulating products of infection and/or inflammation. Another potential mechanism that deserves exploration is that inflammation and/or oxidative stress can modify the known increased risk of oxygen-associated ROP. Taken together, accumulating evidence suggests that prenatal, perinatal, and postnatal systemic inflammation contribute to a 'pre-phase', sensitizing the pre-ROP retina for subsequent insults, setting the stage for what are now called phase I and phase II of ROP pathogenesis. Strategies targeting inflammatory responses might help reduce the risk for ROP in extremely low gestational age newborns.
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