What is Bronchopulmonary Dysplasia (BPD)?

Bronchopulmonary dysplasia (BPD) is a chronic lung condition that primarily affects premature infants who have received mechanical ventilation and oxygen therapy to treat respiratory distress syndrome (RDS). It is characterized by inflammation and injury to the developing lungs, leading to abnormal growth and development of lung tissue.


The condition typically develops in infants born before 28 weeks of gestation or those with very low birth weights. Premature birth interrupts the normal development of the lungs, resulting in underdeveloped alveoli (air sacs) and impaired surfactant production, which are essential for maintaining lung function and oxygen exchange.


What is the relationship between BPD and oxidative stress?

Bronchopulmonary dysplasia (BPD) is associated with increased oxidative stress in premature infants. Oxidative stress occurs when there is an imbalance between the production of reactive oxygen species (ROS) and the body’s ability to detoxify them or repair the resulting damage. Premature infants with BPD are particularly susceptible to oxidative stress due to several factors:


  • Immature antioxidant defenses: Premature infants have underdeveloped antioxidant systems, such as superoxide dismutase, catalase, and glutathione peroxidase, which are crucial for neutralizing ROS and preventing oxidative damage.


  • Oxygen therapy: Infants with BPD often require supplemental oxygen therapy to support breathing due to respiratory insufficiency. However, prolonged exposure to high levels of oxygen can lead to the production of ROS in the lungs, exacerbating oxidative stress and causing further lung injury.


  • Inflammation: Inflammation is a hallmark feature of BPD, characterized by the release of pro-inflammatory cytokines and the infiltration of inflammatory cells into the lung tissue. Inflammatory processes can stimulate the generation of ROS and promote oxidative stress.


  • Ventilator-induced lung injury: Mechanical ventilation, which is commonly used to support breathing in premature infants with respiratory distress, can cause barotrauma and volutrauma to the delicate lung tissue, leading to oxidative stress and lung damage.


  • The oxidative stress associated with BPD can contribute to the pathogenesis and progression of the disease by causing oxidative damage to lipids, proteins, and DNA in the lungs. This damage can impair lung development and function, exacerbate inflammation, and increase susceptibility to respiratory infections. Additionally, oxidative stress can exacerbate other comorbidities commonly observed in premature infants, such as retinopathy of prematurity and neurological impairments.


Therefore, strategies aimed at reducing oxidative stress may have therapeutic potential for preventing or mitigating lung injury and improving outcomes in infants with BPD.