News Release

Discovery sheds light on new strategy to treat some instances of preterm labor

New research published in the Journal of Leukocyte Biology shows that the Notch signaling pathway may be a therapeutic target

Peer-Reviewed Publication

Federation of American Societies for Experimental Biology

A new research report appearing in the August 2016 issue of the Journal of Leukocyte Biology reveals a potentially new therapeutic target for preventing or stopping preterm labor. Specifically, using mice, researchers from the United States show that blocking specific cell signaling pathways may reduce the risk of preterm labor caused by the immune system or inflammation, or stop it altogether. This discovery is important because according to the U.S. National Institute of Child Health and Human Development, NIH, preterm birth is the most common cause of infant death and is the leading cause of long-term disability related to the nervous system in children.

According to Varkha Agrawal, a researcher involved in the work from the NorthShore University HealthSystem in Evanston, Illinois, this report is important because the "identification of key molecules in Notch signaling pathways will pave an approach for therapies to control preterm labor in humans."

To make this discovery, researchers used two mouse models of preterm labor and a control. The first model simulated preterm labor induced via the immune system through the introduction of lipopolysaccharides, which are molecules common in some bacterial infections. The second model simulated preterm labor caused by maternal hormones. In both models, the researchers checked for the expression of genes related to Notch signaling pathways and compared their observations with the controls. The lipopolysaccharide-induced preterm labor group had altered gene expression, while no changes were seen in the normal control mice. The hormonally-induced preterm labor group also had no changes in gene expression in comparison to controls.

"The increased recognition of the link between preterm labor, and inflammation and the immune system opens the door for immunotherapy approaches," said John Wherry, Ph.D., Deputy Editor of the Journal of Leukocyte Biology. "The identification of the role of the Notch pathway specifically is quite exciting since there are known drugs that can modulate this pathway."


The Journal of Leukocyte Biology publishes peer-reviewed manuscripts on original investigations focusing on the cellular and molecular biology of leukocytes and on the origins, the developmental biology, biochemistry and functions of granulocytes, lymphocytes, mononuclear phagocytes and other cells involved in host defense and inflammation. The Journal of Leukocyte Biology is published by the Society for Leukocyte Biology.

Details: Varkha Agrawal, Mukesh K. Jaiswal, Sahithi Pamarthy, Gajendra K. Katara, Arpita Kulshrestha, Alice Gilman-Sachs, Emmet Hirsch, and Kenneth D. Beaman. Role of Notch signaling during lipopolysaccharide-induced preterm labor. J. Leukoc. Biol. August 2016, 100:261-274; doi:10.1189/jlb.3HI0515-200RR ; ; Early online version: September 15, 2015; Final version: August 1, 2016

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