Researchers at the National Institutes of Health (NIH) have recently reported that the gene variants in the mother and the fetus play a notable role in the risk of pre-term labor – one of the main causes of infant disability and mortality.

Presenting the study at the 30th Annual Society for Material-Fetal Medicine in Chicago, NIH’s Dr. Roberto Romero noted that genes in the mother and fetus can increase the chances of vulnerability to an inflammatory response to infections inside the uterus.

The findings of the study were based on the researchers’ comprehensive analysis of 190 genes and over 700 DNA variants from 229 mothers and 179 infants born pre-term in Chile; and the genes of 600 mothers who delivered babies after a full-term pregnancy.

The researchers found that the strongest gene influences in the fetus and the mother respectively were ‘interleukin 6’ receptor and ‘tissue inhibitor of metalloproteinase 2,’ or TIMP2. While the fetus’ gene is essentially involved in the body’s response to inflammation; the mother’s gene affects structures in the cervix and uterus that get broken down at the onset of labor.

Explaining the role of these genes in pre-term deliveries, Romero said that in case of an infection, the combination of these two genetic profiles increase the pre-term labor risk, as the body tries to save the lives of the mother and the baby.