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NIH scientists identify maternal and fetal genes that increase preterm birth risk
Date:2/4/2010

issues. The maternal and fetal genes that Dr. Romero and his colleagues identified regulate the amount of extracellular matrix in the uterus. The extracellular matrix of the uterine cervix and of the membranes containing the embryonic fluid are broken down at the beginning of labor.

To conduct the study, the scientists evaluated 190 genes and more than 700 DNA variants in samples from 229 women and 179 premature infants, and a large number of women who delivered at term. The study was conducted on a population of women in Chile. All of the women in the study were of Hispanic origin (of largely white and Native American backgrounds.). The study is one of the few to look at the genetic factors governing birth in an exclusively Hispanic population.

Infants who carried the DNA variant in the gene for the Interleukin 6 receptor were more likely to be born premature than those who did not. Interleukin 6 is produced by cells in response to infection and is involved in inflammation. In previous studies, Dr. Romero and his team found that high levels of Interleukin 6 in the amniotic fluid and in the fetal blood are associated with the beginning of premature labor.

Dr. Romero noted that molecules responsible for inflammation such as Interleukins 1 and 6 predate the human species and even mammals. He added that Interleukin 1-like molecules are even present in primitive organisms, such as sponges (which do not undergo labor). The primary function of these molecules is to fight infection. However, in most mammals, these molecules are not only used by the immune system to fight infection, but also play a role in triggering the onset of labor.


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Contact: Robert Bock
bockr@mail.nih.gov
301-496-5133
NIH/National Institute of Child Health and Human Development
Source:Eurekalert

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