Chorioamnionitis and Early Lung Inflammation in Infants in Whom Bronchopulmonary Dysplasia Develops

Abstract

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 2000 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 1β(IL-1β), 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-1β from the first day of intubation and the development of BPD. Tracheal lavage concentrations of IL-1β 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 2000 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.

Placental Neutrophil Infiltration Associated with Tobacco Exposure but Not Development of Bronchopulmonary Dysplasia

“…Though a previous study showed a potential association of BPD with maternal tobacco exposure, the majority of the literature indicates that maternal smoking during pregnancy is not an independent risk factor for BPD development, after controlling for additional variables [6,8,32,33]. With the exception of antepartum hemorrhage incidence, which was significantly higher in the composite outcome group compared to the No BPD group (46.7% vs. 4.2%; p = 0.003), we found no difference in known risk factors for BPD, including maternal hypertension, PPROM, and chorioamnionitis [8][9][10][11][12]. In line with other studies [7], infants with the composite outcome of BPD or death had a lower gestational age and birth weight compared to infants in the No BPD group.…”

“…BPD is the most prevalent sequela of preterm birth, affecting 10,000-15,000 infants annually in the United States [7]. Known postnatal risk factors for the disease include hyperoxia, mechanical ventilation, patent ductus arteriosus (PDA), and sepsis; antenatal risk factors include chorioamnionitis, preeclampsia, and hypertension [8][9][10][11][12].…”

A comparative immunohistochemical investigation of the consequences of chorioamnionitis on the developing human fetal spleen

“…A recent in-depth review of the literature revealed that the majority of fetuses exposed to chorioamnionitis develop a systemic inflammatory response known as the fetal inflammatory response syndrome (FIRS) [50,51]. Chorioamnionitis affects multiple organ systems such as the heart, causing abnormal fetal cardiac function [52], the brain causing developmental delay and lifelong neurological impairments [53 -55], the lungs causing a reduced risk of developing respiratory distress syndrome (RDS) and an increased risk of bronchopulmonary dysplasia (BPD) [56], the retina causing retinopathy of prematurity (ROP) [57,58], the kidneys causing oligohydramnios and resulting in reduction of fetal renal function, and finally it is obvious that uncontrolled situation could lead to sepsis [59][60]. Recently, Galinsky et al, have demonstrated that preterm fetal sheep exposed to intrauterine inflammation had a reduction in nephron number of approximately 20% [61].…”

Biological markers in cord blood for prediction of bronchopulmonary dysplasia in premature infants

“…It is often accompanied with the evidence of the invasion of pathogenic bacteria into normal tissues [15,16]. HCA reduces the incidence rate of RDS in infants with birth weight < 2,000 g but increases the incidence of chronic pulmonary disease [17]. This finding indicates that HCA promotes pulmonary maturation by stimulating adrenal function to promote cortisol secretion on the one hand [18]; on the other, intrauterine infection-induced fetal inflammation significantly disturbs the normal development of the pulmonary structure [19].…”