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Chorioamnionitis and early lung inflammation in infants in whom bronchopulmonary dysplasia develops
K L Watterberg1, L M Demers, S M Scott
1Department of Pediatrics, Milton S. Hershey Medical Center, Pennsylvania State University, Hershey 17033, USA.
Insights
Prenatal inflammation, specifically chorioamnionitis, may be a primary cause of bronchopulmonary dysplasia (BPD) in premature infants. This inflammation, evident from the first day of life, contributes to lung injury and the development of BPD.
Area of Science:
- Neonatal Medicine
- Respiratory Medicine
- Pediatric Pathology
Background:
- Bronchopulmonary dysplasia (BPD) is often linked to mechanical ventilation and oxygen therapy in premature infants.
- Early lung inflammation in BPD has been considered a consequence of these interventions.
Purpose of the Study:
- To investigate whether prenatal inflammation, specifically chorioamnionitis, is a primary causative factor in BPD development.
- To evaluate the role of prenatal inflammation in neonatal lung injury.
Main Methods:
- Prospective enrollment of intubated newborns weighing less than 2,000g.
- Documentation of chorioamnionitis and assessment of lung inflammation via tracheal lavage cytokine analysis (IL-1 beta, thromboxane B2, etc.) on days 1, 2, and 4.
- Comparison of inflammatory markers between infants who developed BPD and those who did not.
Main Results:
- Chorioamnionitis was significantly associated with increased IL-1 beta levels from day 1 and the development of BPD.
- Infants who developed BPD showed higher IL-1 beta concentrations.
- Elevated thromboxane B2 levels were observed on days 2 and 4 in infants with BPD.
Conclusions:
- Intubated infants with BPD exhibited increased prenatal inflammatory exposure (chorioamnionitis) and elevated lung inflammation from the first postnatal day.
- Chorioamnionitis may accelerate lung maturation but also induces inflammation and injury, contributing to BPD development in intubated infants.
Objective:
The development of bronchopulmonary dysplasia (BPD) often has been attributed to injury from mechanical ventilation and supplemental oxygen. Early lung inflammation in infants with BPD has been thought to be secondary to these factors. The purpose of this study was to evaluate whether preexisting (prenatal) inflammation may be a primary causative factor in the development of BPD.
Methods:
Intubated newborns of less than 2,000 g birth weight were prospectively enrolled. The presence or absence of chorioamnionitis was documented. Lung inflammation was evaluated on days 1, 2, and 4 of intubation by assaying concentrations of interleukin 1 beta (IL-1 beta), thromboxane B2, leukotriene B4, and prostaglandin E2 in tracheal lavages. Infants in whom BPD developed were compared with those in whom it did not using these measures.
Results:
Fifty-three infants were enrolled; 41 survived. Thirty-eight had respiratory distress syndrome; 15 were intubated for other diagnoses. Infants prenatally exposed to chorioamnionitis were less likely to present with respiratory distress syndrome; however, chorioamnionitis was significantly associated with both the presence of IL-1 beta from the first day of intubation and the development of BPD. Tracheal lavage concentrations of IL-1 beta were higher in infants in whom BPD developed. Thromboxane B2 concentrations were similar on day 1 but were higher on days 2 and 4 in infants in whom BPD developed.
Conclusions:
In this study, intubated infants weighing less than 2,000 g at birth in whom BPD developed had increased exposure to inflammation prenatally (chorioamnionitis) and evidence of increased lung inflammation from the first postnatal day. We speculate that chorioamnionitis may accelerate lung maturation but that it also causes lung inflammation and subsequent lung injury in intubated infants, fostering the development of BPD.