WSU mice assist with therapies for preventing pre-term birth

Preterm birth is the leading cause of neonatal mortality worldwide.  One out of four preterm infants are born to a woman with an intra-amniotic infection or inflammation process, yet there is no clinical treatment for this condition. In Drs. Jose Galaz and Nardhy Gomez-Lopez (et al.) recent 2022 paper, “Clarithromycin prevents preterm birth and neonatal mortality by dampening alarmin-induced maternal-fetal inflammation in mice”, they investigated the potential therapeutic effects of clarithromycin on adverse neonatal outcomes in mice. The importance of this relationship is in a potential treatment and prevention for preterm birth and the results have been featured by the National Institutes of Child Health and Human Development.

Their data suggest that clarithromycin reduces the placental inflammation induced by an intra-amniotic protein (HMGB1), providing a potential mechanism to improve neonatal survival. Treatment with clarithromycin dampened inflammation in fetal mouse tissues, namely lung, intestine, and liver. According to Dr. Jose Galaz, “Clarithromycin is a macrolide antibiotic that is approved to be used in pregnant women, and thus our results support the potential use of clarithromycin to treat pregnant women with sterile intra-amniotic inflammation.” This paper represents the first published evidence showing the anti-inflammatory effects of clarithromycin on intra-amniotic inflammation and neonatal survival and has potentially important implications for preterm labor and birth. 

This work was performed at the Maternal-Fetal Immunobiology Unit of the Perinatology Research Branch. For more information and a link to the full article, click below:

Clarithromycin prevents preterm birth and neonatal mortality by dampening alarmin-induced maternal–fetal inflammation in mice - PMC (

This research was supported by the Perinatology Research Branch, Division of Obstetrics and Maternal–Fetal Medicine, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, U.S. Department of Health and Human Services (NICHD/NIH/DHHS) under Contract No. HHSN275201300006C (R.R.). This research was also supported by the Wayne State University Perinatal Initiative in Maternal, Perinatal and Child Health (N.G.-L.). The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

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