Potential Link Between the Immune System and Premature Birth
PREMATURE birth is a major cause of infant death and disability, with around 337,000 babies born prematurely in the USA in 2016. A link between the immune system and premature birth has been proposed based on a study conducted in the USA.
Based on previous research, which had shown that cytokines were present in the amniotic fluid of a significant number of women who gave birth prematurely, researchers developed a hypothesis: “There are a lot of anti-inflammatory mechanisms that prevent the fetus from being rejected. So, we thought maybe dangerous inflammation that can break down the tolerance barrier could mediate the start-up of birth,” explained one of the study’s authors, Dr Anthony Vella, Department of Pediatrics, University of Connecticut School of Medicine, Farmington, Connecticut, USA.
The researchers initially exposed cells from the female reproductive tract and the amniotic fluid to bacteria in the laboratory. They were surprised to discover that this stimulated far higher levels of granulocyte-macrophage colony-stimulating factor (GM-CSF) than they had expected. Following this discovery, the researchers then conducted a study using a mouse model to study this further.
Researchers gave one group of mice lipopolysaccharide, which increased GM-CSF concentration, and a GM-CSF antibody and gave a second group of mice lipopolysaccharide and a control antibody. Six hours post treatment, the researchers began to record the preterm birth rate, and found that the control group (administered GM-CSF and a control antibody) had a preterm birth rate of 66.7%, while the group receiving the GM-CSF antibody had a preterm birth rate of 25%.
There are several steps that need to be undertaken before this potential connection between the immune system and premature birth can result in beneficial findings for human patients, but the results open an intriguing research avenue that may allow preterm births to be presented. Further immune mechanism studies are planned in mice before initiating studies in humans.