Bronchopulmonary Dysplasia andUreaplasma: What Do We Know So Far?

Abstract

Bronchopulmonary dysplasia (BPD) is the most common morbidity of prematurity. BPD is a chronic respiratory disease related to lung-injury during the primary course of critical lung disease such as respiratory distress syndrome or when abnormal development of the preterm lung occurs. Abnormal lung development not only results from primary lung injury in the first days after birth, but also secondary injury through abnormal repair resulting in arrested and abnormal alveolarization, fibrosis and pulmonary vascular dysgenesis. Chorioamnionitis is a risk factor that plays an important role in the development of BPD. Ureaplasma subspecies (spp.) are the most common isolated organisms from chorioamniotic tissue after premature births. Therefore Ureaplasma spp. appear to play an important role in the development of BPD, and treatment or prophylactic treatment of these infections or coloni zation may reduce the incidence, morbidity and mortality of BPD. Ureaplasma spp. infections are challenging not only to treat, but also to diagnosis in a timely manner. This review summarizes the current state of treatment and new developments in the treatment of Ureaplasma exposure in premature infants.

Pathophysiological mechanisms and pharmacological methods of prevention and treatment of bronchopulmonary dysplasia in preterm infants

“…Concerning premature infants, impaired activity of antioxidative enzymes, such as catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), results in the accumulation of ROS, and thus direct damage to the surfactant, destruction of type I pneumocytes and damage to the barrier capillary-vesicular [2,5,18] Chorioamnionitis and perinatal infection, mainly caused by Ureaplasma urealyticum and Chlamydia trachomatis, positively correlate with the incidence of BPD in premature infants, most likely by stimulating the synthesis and secretion of epithelial cells of the respiratory system chemotactic factors for polymorphonuclear leukocytes, mainly ENA-78 epithelial protein and IL-8, as well as by inducing protein chemotactic factors released by macrophages, such as macrophage inflammatory protein (MIP-1) [5,[19][20][21][22] Intrauterine infection or perinatal infection caused by Ureaplasma urealyticum causes an increased inflammatory response in the lungs, which disturbs the maturation and differentiation of alveoli and, on the other hand, significantly increases fibrosis [23,24]. In lung specimens collected from animals infected with Ureaplasma urealitycum, concentrations of interferon gamma (IFN-γ), TNF-α, transforming growth factor (TGF-1β) and IL-1β, were significantly higher compared to healthy organisms [25,26].…”