A study led by researchers at the University of Washington School of Medicine in Seattle shows that, in preterm animal models, inflammation due to infection can disrupt the activity of genes that are crucial for normal development of the heart. The study findings were published in the American Journal of Obstetrics & Gynecology . 

Dr. Kristina Adams Waldorf lead author, "This study connects the dots between  preterm birth  and heart disease in adult life by defining the gene networks disrupted by infection and inflammation that program normal heart development."

She said, "We talked to women in preterm labor about the risk to their infants of lung and brain injury." We now know that long-term health risks of a preterm birth extend beyond the developing lungs and brain to involve vision, hearing, kidney and even heart function. "

Dr. Kristina Adams Waldorf, a professor of obstetrics and gynecology at the University of Washington School of Medicine explained how bacterium infections in the uterus during pregnancy can disrupt gene activity essential for heart formation in the fetus and lead to heart disease later in life Credit: UW Medicine

"This study is the first to show that the gene program for heart development in preterm babies is interrupted in preterm babies exposed to fetal infection and inflammation, which may lead to incomplete heart development," said Mitchell. "This incomplete development, in turn, may lead to the higher risk of abnormal heart rhythms and heart failure seen when preterm babies reach adulthood."

The researchers studied the heart tissue from fetal pigtail macaque monkeys whose mothers' uteruses had been infected with bacteria, namely Group B Streptococcus and Escherichia coli. These often cause infections in human mothers and trigger preterm birth.

The investigators compared gene expression from fetal heart tissues infected with bacteria to normal heart tissues. The infections in these experiments were severe, a scenario that is typical of early preterm births , which occurs in approximately 2% of all US births. Infection triggered a marked inflammatory response in the fetus.

Inflammation was also present in the heart tissues and characterized by elevations in inflammatory proteins, like interleukin-6 and interleukin 8. Many of the genes with altered expression-NPPA, MYH6 and ACE2-have known functions in heart development or are linked to heart disease . 

The researchers also found significant alteration in the expression of gene networks involved in heart and blood vessel formation, "These findings suggest that many pathways related to fetal heart development may be impacted by inflammation and infection," said Mitchell.

"Future research should investigate whether combining antibiotics to treat the infection and anti-inflammatory drugs can lessen inflammation and damage to the fetal heart ," noted Adams Waldorf. "If we can better understand how to prevent infections that cause preterm birth, we can protect fetuses and enhance their long-term health into adulthood ."