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Neuroinflammation contributes to developmental brain injury associated with preterm birth, but the mediators that drive it are incompletely understood. Previous studies have shown that complement C5a is present and injurious in the brains of foetal mice exposed to preterm labour. Here, we demonstrate that C5a is present in the cerebrospinal fluid of newborn human infants and that levels are elevated in those born preterm. The difference is not explained by systemic infection. Complement activation in the neonatal brain and its role as a potential therapeutic target in preterm brain injury warrant further study. Activation in the neonatal brain and its role as a potential therapeutic target for preterm brain injury warrants further study.

Citation

Rozalia Pataky, Forbes A Howie, Guillermina Girardi, James P Boardman. Complement C5a is present in CSF of human newborns and is elevated in association with preterm birth. The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians. 2017 Oct;30(20):2413-2416

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PMID: 27806664

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