Bronchopulmonary dysplasia (BPD) is a lung condition that occurs in infants, especially in premature infants. BPD is characterized by abnormal lung development and inflammation and scarring in the lungs. It is one of the most common lung diseases in children, with 5,000 to 10,000 new cases each year in the United States.
The exact cause of BPD is still being studied. Researchers do know that the condition develops from irritation or inflammation in the lungs. Additionally, some research suggests that the genes you are born with play a role in BPD.
Premature infants are at an increased risk of BPD because they have very fragile lungs which are more susceptible to irritation and inflammation. Ventilator support and oxygen therapy are both common in premature infants and can both lead to irritation and inflammation in the lungs.
An important aspect in both BPD and premature infants is the increased risk of disruption of angiogenesis. Angiogenesis is an important process in which the body creates new blood vessels from pre-existing ones. This process is required for normal growth and development and for proper wound healing. Disruption of this process can increase inflammation and scarring in the lungs, thereby increasing risk for BPD.
In a recent animal study, researchers examined if vitamin D has a role in BPD. Research suggests that vitamin D has some kind of role in lung function. Vitamin D has been shown to reduce inflammation and it has been suggested to play a role in conditions such as asthma, chronic obstructive pulmonary disease and cystic fibrosis.
In the current study, researchers wanted to know if vitamin D might help reduce inflammation in BPD and/or help prevent it.
The researchers looked at the effects of vitamin D on markers of BPD and impaired lung growth in 101 infant rats. Fifty-four rat pups were injected with what is called endotoxin (ETX). Exposure to ETX inhibits lung growth in infant rats. ETX is a toxic substance in bacterial cells that is released when the cell ruptures. ETX can cause alterations in the normal functioning of angiogenesis in the lung.
Twenty-seven infant rats were injected with ETX and vitamin D. And twenty rat infants served as controls and were not injected with anything. The infant rats received these injections 2 days before birth to mimic the stage of human lung development in high BPD risk premature newborns born at 24 to 26 weeks. They then were monitored for two weeks before analysis of different factors associated with lung growth. Here’s what the researchers found:
- Vitamin D treatment in ETX-exposed rat pups on day 1 had survival rates of 84% compared to 52% in the rat pups only exposed to ETX and on day 3 also had survival rates of 84% compared to 42% in the rat pups only exposed to ETX (p<0.001).
- Vitamin D treatment in ETX-exposed rat pups improved alveolar type II cell growth to levels similar to the control rat pups. Alveolar type II cells secrete pulmonary surfactant which helps the lungs and thorax to expand. In premature infants, like the rat pups in this study, alveolar type II cell growth is reduced and adequate amounts of pulmonary surfactant have not been secreted which can affect lung growth and function.
- Vitamin D treatment in ETX-exposed rat pups decreased right ventricular hypertrophy. Right ventricular hypertrophy occurs when not enough blood is pumped from the right ventricle to the lungs.
- Pulmonary artery endothelial cell growth in cells exposed to ETX alone decreased by 50% at baseline. However, in cells exposed to both ETX and vitamin D, the decrease wasn’t as severe and closer to controls (p<0.001). Pulmonary artery endothelial cells are the cells in the arteries of the lungs. They help with lung circulation through the maintenance of pressure and by the regulation of the amount of fluids and solutes that come into the lungs. A reduction in these cells can alter the balance in the lungs and cause angiogenesis to not function properly.
The researchers conclude,
“Vitamin D has proliferative and protective effects on fetal pulmonary artery endothelial cells and alveolar type II cells, and prevents abnormal infant lung structure in an experimental model of chorioamnionitis. We speculate that decreased vitamin D activity may contribute to the pathogenesis of BPD and that early vitamin D therapy may provide a potential strategy for the prevention of BPD in at risk preterm infants.”
The researchers also note limitations in their study. First, a single injection of ETX might not accurately represent what might occur in human preterm infants. Additionally, ETX exposure may only explain one part of the complex nature of BPD.
This being an animal study means the results should be taken with caution. While this study shows that vitamin D may help with various factors of lung growth and inflammation, we still need to learn more about how vitamin D impacts lung conditions. More research is needed on the relationship between BPD and vitamin D, including experiments in humans.
Mandell, E. et al. Vitamin D Treatment Improves Survival and Infant Lung Structure After Intra-Amniotic Endotoxin Exposure in Rats: Potential Role for the Prevention of Bronchopulmonary Dysplasia. American Journal of Physiology, 2014.