Senad Divanovic, PhD
Scientists at Cincinnati Children’s have identified a molecular driver of inflammation that may finally answer a key question about what causes mild systemic prenatal infections to trigger preterm birth.
The findings, published March 9, 2017, in The Journal of Clinical Investigation, may lead to new approaches to address an entrenched global health problem.
Researchers say a molecular signaling receptor that helps regulate the immune system, type I Interferon (IFNAR), signals when a woman may have a mild viral or bacterial infection that could trigger infection-driven preterm birth.
In mouse models, deleting or neutralizing the IFNAR receptor protected the animals from preterm birth.
“Preterm birth is a leading worldwide cause of illness and death in infants,” says Senad Divanovic, PhD, lead investigator on the study and a member of Division of Immunobiology. “Identifying active type I IFN/IFNAR as an immunological driver provides an actionable biomarker and potential therapeutic target for reducing preterm birth risk in these circumstances.”